TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Trajković, Vladimir S.
AU  - Maksimović-Ivanić, Danijela
AU  - Samardžić, Tatjana S.
PY  - 2002
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/532
AB  - The ability of interleukin-17 (IL-17) to induce nitric oxide (NO) synthesis in murine L929 fibroblasts was investigated. L929 cells were incubated with IL-17 and/or LPS, interferon-g (IFN-gama), interleukin-1 (IL-1), or dibutyryl-cAMP. NO production was assessed indirectly, by measuring nitrite accumulation in 24 h culture supernatants. L929 fibroblasts did not produce NO constitutively, nor IL-17 alone induced NO production. Of all other stimuli tested, only IFN-gama significantly up regulated nitrite level in L929 cell cultures. However, when IL-17 was applied simultaneously with each of the tested stimuli, NO synthesis was markedly elevated, thus indicating involvement of distinct signaling pathways of NO induction by IL-17 and other tested agents. Production of NO by IL-17+LPS-treated L929 cells was dependent on synthesis and activity of inducible NO synthase (iNOS), as indicated by abrogation of nitrite accumulation with protein synthesis inhibitor cycloheximide or selective inhibitor of iNOS, aminoguanidine. A role for protein tyrosine kinase (PTK) and transcription factor NF-kB in iNOS activation is suggested by reduction of NO synthesis with PTK inhibitor genistein and an inhibitor of NF-kB activation, pyrrolidine dithiocarbamate (PDTC). In contrast, protein kinase C inhibitor staurosporine was ineffective in blocking IL-17+LPS-induced NO production in L929 cells. Taken together, our results for the first time showed an active participation of IL-17 in co-induction of fibroblast NO synthesis with LPS, cytokines (IL-1, IFN-gama), or cAMP analogue, and suggested that IL-17 up-regulated NO synthesis in fibroblasts through mechanisms involving PTK and NF-kB activation.
AB  - Ispitan je uticaj interleukina-17 (IL-17) na produkciju azot monoksida (NO) od strane L929 fibroblasta. L929 ćelije su inkubirane sa IL-17 i/ili LPS-om, interferonom-gama (IFN-gama), interleukinom-1 (IL-1), ili dibutiril-cAMP-om. Produkcija NO ispitana je indirektno, merenjem koncentracije nitrita akumuliranih nakon 24 h u supernatantu ćelijskih kultura. Kultivisani L929 fibroblasti nisu produkovali NO konstitutivno, niti je sam IL-17 indukovao NO produkciju. Od ostalih ispitanih agenasa samo je IFN-gama značajno povećao nivo nitrita u kulturama L929 ćelija. Međutim, kada je IL-17 primenjen sa bilo kojim od testiranih agenasa, došlo je do snažnog povećanja NO sinteze, što je ukazalo da su signalni putevi indukcije NO sa IL-17 i ostalim navedenim agensima različiti. Sprečavanje akumulacije nitrita inhibitorom proteinske sinteze cikloheksimidom ili selektivnim inhibitorom iNOS aminoguanidinom u ćelijama stimulisanim sa IL-17+LPS ukazalo je da NO produkcija zavisi od sinteze i aktivnosti enzima inducibilne NO sinteze (iNOS). Inhibitor protein tirozin kinaze (PTK), genistein i inhibitor aktivacije transkripcionog faktora NF-kB, pirolidin ditiokarbamat (PDTC), takođe su redukovali sintezu NO. Nasuprot tome, inhibitor protein kinaze C, staurosporin, nije blokirao NO produkciju L929 ćelija stimulisanih sa IL-17+LPS. U celini, naši rezultati su po prvi put pokazali aktivno učešće IL-17 u koindukciji NO sinteze sa LPS-om, citokinima (IL-1, IFN-gama), ili cAMP analogom u fibroblastima i ukazali da stimulacija NO sinteze sa IL-17 uključuje mehanizme zavisne od PTK i NF-kB.
PB  - Beograd: Institut za reumatologiju
T2  - Acta rheumatologica Belgradensia
T1  - Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta
T1  - Effect of interleukin-17 on nitric oxide production in murine fibroblast-like cell line L929
IS  - 1
VL  - 32
SP  - 1
EP  - 10
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_532
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Trajković, Vladimir S. and Maksimović-Ivanić, Danijela and Samardžić, Tatjana S.",
year = "2002, 2002",
abstract = "The ability of interleukin-17 (IL-17) to induce nitric oxide (NO) synthesis in murine L929 fibroblasts was investigated. L929 cells were incubated with IL-17 and/or LPS, interferon-g (IFN-gama), interleukin-1 (IL-1), or dibutyryl-cAMP. NO production was assessed indirectly, by measuring nitrite accumulation in 24 h culture supernatants. L929 fibroblasts did not produce NO constitutively, nor IL-17 alone induced NO production. Of all other stimuli tested, only IFN-gama significantly up regulated nitrite level in L929 cell cultures. However, when IL-17 was applied simultaneously with each of the tested stimuli, NO synthesis was markedly elevated, thus indicating involvement of distinct signaling pathways of NO induction by IL-17 and other tested agents. Production of NO by IL-17+LPS-treated L929 cells was dependent on synthesis and activity of inducible NO synthase (iNOS), as indicated by abrogation of nitrite accumulation with protein synthesis inhibitor cycloheximide or selective inhibitor of iNOS, aminoguanidine. A role for protein tyrosine kinase (PTK) and transcription factor NF-kB in iNOS activation is suggested by reduction of NO synthesis with PTK inhibitor genistein and an inhibitor of NF-kB activation, pyrrolidine dithiocarbamate (PDTC). In contrast, protein kinase C inhibitor staurosporine was ineffective in blocking IL-17+LPS-induced NO production in L929 cells. Taken together, our results for the first time showed an active participation of IL-17 in co-induction of fibroblast NO synthesis with LPS, cytokines (IL-1, IFN-gama), or cAMP analogue, and suggested that IL-17 up-regulated NO synthesis in fibroblasts through mechanisms involving PTK and NF-kB activation., Ispitan je uticaj interleukina-17 (IL-17) na produkciju azot monoksida (NO) od strane L929 fibroblasta. L929 ćelije su inkubirane sa IL-17 i/ili LPS-om, interferonom-gama (IFN-gama), interleukinom-1 (IL-1), ili dibutiril-cAMP-om. Produkcija NO ispitana je indirektno, merenjem koncentracije nitrita akumuliranih nakon 24 h u supernatantu ćelijskih kultura. Kultivisani L929 fibroblasti nisu produkovali NO konstitutivno, niti je sam IL-17 indukovao NO produkciju. Od ostalih ispitanih agenasa samo je IFN-gama značajno povećao nivo nitrita u kulturama L929 ćelija. Međutim, kada je IL-17 primenjen sa bilo kojim od testiranih agenasa, došlo je do snažnog povećanja NO sinteze, što je ukazalo da su signalni putevi indukcije NO sa IL-17 i ostalim navedenim agensima različiti. Sprečavanje akumulacije nitrita inhibitorom proteinske sinteze cikloheksimidom ili selektivnim inhibitorom iNOS aminoguanidinom u ćelijama stimulisanim sa IL-17+LPS ukazalo je da NO produkcija zavisi od sinteze i aktivnosti enzima inducibilne NO sinteze (iNOS). Inhibitor protein tirozin kinaze (PTK), genistein i inhibitor aktivacije transkripcionog faktora NF-kB, pirolidin ditiokarbamat (PDTC), takođe su redukovali sintezu NO. Nasuprot tome, inhibitor protein kinaze C, staurosporin, nije blokirao NO produkciju L929 ćelija stimulisanih sa IL-17+LPS. U celini, naši rezultati su po prvi put pokazali aktivno učešće IL-17 u koindukciji NO sinteze sa LPS-om, citokinima (IL-1, IFN-gama), ili cAMP analogom u fibroblastima i ukazali da stimulacija NO sinteze sa IL-17 uključuje mehanizme zavisne od PTK i NF-kB.",
publisher = "Beograd: Institut za reumatologiju",
journal = "Acta rheumatologica Belgradensia",
title = "Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta, Effect of interleukin-17 on nitric oxide production in murine fibroblast-like cell line L929",
number = "1",
volume = "32",
pages = "1-10",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_532"
}

Stošić-Grujičić, S., Trajković, V. S., Maksimović-Ivanić, D.,& Samardžić, T. S.. (2002). Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta. in Acta rheumatologica Belgradensia
Beograd: Institut za reumatologiju., 32(1), 1-10.
https://hdl.handle.net/21.15107/rcub_ibiss_532

Stošić-Grujičić S, Trajković VS, Maksimović-Ivanić D, Samardžić TS. Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta. in Acta rheumatologica Belgradensia. 2002;32(1):1-10.
https://hdl.handle.net/21.15107/rcub_ibiss_532 .

Stošić-Grujičić, Stanislava, Trajković, Vladimir S., Maksimović-Ivanić, Danijela, Samardžić, Tatjana S., "Uticaj interleukina-17 na produkciju azot monoksida (NO) od strane L929 ćelijske linije mišijih fibroblasta" in Acta rheumatologica Belgradensia, 32, no. 1 (2002):1-10,
https://hdl.handle.net/21.15107/rcub_ibiss_532 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Drulović, Jelena S
AU  - Trajković, Vladimir S
AU  - Mesaros, Sarlota
AU  - Dujmović, Irena
AU  - Maksimović-Ivanić, Danijela
AU  - Samardžić, Tatjana S.
AU  - Stojsavljević, Nebojsa
AU  - Lević, Zvonimir
AU  - Mostarica-Stojković, Marija B
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1791
AB  - Interleukin-6 (IL-6) and nitric oxide (NO) are implicated in the pathology of multiple sclerosis (MS). We have investigated the levels of these mediators in the cerebrospinal fluid (CSF) from 50 patients with MS and 23 control subjects. Mean CSF IL-6 level was higher in the total MS group in comparison with controls, but not significantly, whilst the difference between patients with stable MS and controls reached the level of statistical significance. Mean CSF nitrite/nitrate level was significantly higher in the total MS group compared with the control group, as well as in active MS patients versus controls. There was significant difference neither in the mean CSF IL-6 nor in nitrite/nitrate levels between active and stable MS patients. Interestingly, we observed a significant negative correlation between IL-6 and nitrite/nitrate levels in the CSF in the total MS group. Such a trend existed in both subgroups with active and stable MS, but without reaching the level of statistical significance. Our data further support the involvement of IL-6 and NO in ongoing pathological processes in MS, suggesting their potential interplay within the central nervous system in this disease.
PB  - John Wiley and Sons
T2  - European Journal of Neurology
T1  - Nitric oxide metabolites and interleukin-6 in cerebrospinal fluid from multiple sclerosis patients
IS  - 4
VL  - 9
DO  - 10.1046/j.1468-1331.2002.00437.x
SP  - 413
EP  - 418
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1791
ER  - 

@article{
author = "Miljković, Đorđe and Drulović, Jelena S and Trajković, Vladimir S and Mesaros, Sarlota and Dujmović, Irena and Maksimović-Ivanić, Danijela and Samardžić, Tatjana S. and Stojsavljević, Nebojsa and Lević, Zvonimir and Mostarica-Stojković, Marija B",
year = "2002",
abstract = "Interleukin-6 (IL-6) and nitric oxide (NO) are implicated in the pathology of multiple sclerosis (MS). We have investigated the levels of these mediators in the cerebrospinal fluid (CSF) from 50 patients with MS and 23 control subjects. Mean CSF IL-6 level was higher in the total MS group in comparison with controls, but not significantly, whilst the difference between patients with stable MS and controls reached the level of statistical significance. Mean CSF nitrite/nitrate level was significantly higher in the total MS group compared with the control group, as well as in active MS patients versus controls. There was significant difference neither in the mean CSF IL-6 nor in nitrite/nitrate levels between active and stable MS patients. Interestingly, we observed a significant negative correlation between IL-6 and nitrite/nitrate levels in the CSF in the total MS group. Such a trend existed in both subgroups with active and stable MS, but without reaching the level of statistical significance. Our data further support the involvement of IL-6 and NO in ongoing pathological processes in MS, suggesting their potential interplay within the central nervous system in this disease.",
publisher = "John Wiley and Sons",
journal = "European Journal of Neurology",
title = "Nitric oxide metabolites and interleukin-6 in cerebrospinal fluid from multiple sclerosis patients",
number = "4",
volume = "9",
doi = "10.1046/j.1468-1331.2002.00437.x",
pages = "413-418",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1791"
}

Miljković, Đ., Drulović, J. S., Trajković, V. S., Mesaros, S., Dujmović, I., Maksimović-Ivanić, D., Samardžić, T. S., Stojsavljević, N., Lević, Z.,& Mostarica-Stojković, M. B.. (2002). Nitric oxide metabolites and interleukin-6 in cerebrospinal fluid from multiple sclerosis patients. in European Journal of Neurology
John Wiley and Sons., 9(4), 413-418.
https://doi.org/10.1046/j.1468-1331.2002.00437.x
https://hdl.handle.net/21.15107/rcub_ibiss_1791

Miljković Đ, Drulović JS, Trajković VS, Mesaros S, Dujmović I, Maksimović-Ivanić D, Samardžić TS, Stojsavljević N, Lević Z, Mostarica-Stojković MB. Nitric oxide metabolites and interleukin-6 in cerebrospinal fluid from multiple sclerosis patients. in European Journal of Neurology. 2002;9(4):413-418.
doi:10.1046/j.1468-1331.2002.00437.x
https://hdl.handle.net/21.15107/rcub_ibiss_1791 .

Miljković, Đorđe, Drulović, Jelena S, Trajković, Vladimir S, Mesaros, Sarlota, Dujmović, Irena, Maksimović-Ivanić, Danijela, Samardžić, Tatjana S., Stojsavljević, Nebojsa, Lević, Zvonimir, Mostarica-Stojković, Marija B, "Nitric oxide metabolites and interleukin-6 in cerebrospinal fluid from multiple sclerosis patients" in European Journal of Neurology, 9, no. 4 (2002):413-418,
https://doi.org/10.1046/j.1468-1331.2002.00437.x .,
https://hdl.handle.net/21.15107/rcub_ibiss_1791 .

TY  - CONF
AU  - Stošić-Grujičić, Stanislava
AU  - Trajković, Vladimir S
AU  - Miljković, Đorđe
AU  - Stojanović, Ivana D.
AU  - Maksimović-Ivanić, Danijela
AU  - Samardžić, Tatjana S.
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1794
C3  - Clinical Immunology
T1  - Cell-specific effect of inerleukin-17 (IL-17) in inducible nitric oxide synthase (iNOS) activation.
IS  - 3
VL  - 103
EP  - S22
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1794
ER  - 

@conference{
author = "Stošić-Grujičić, Stanislava and Trajković, Vladimir S and Miljković, Đorđe and Stojanović, Ivana D. and Maksimović-Ivanić, Danijela and Samardžić, Tatjana S.",
year = "2002",
journal = "Clinical Immunology",
title = "Cell-specific effect of inerleukin-17 (IL-17) in inducible nitric oxide synthase (iNOS) activation.",
number = "3",
volume = "103",
pages = "S22",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1794"
}

Stošić-Grujičić, S., Trajković, V. S., Miljković, Đ., Stojanović, I. D., Maksimović-Ivanić, D.,& Samardžić, T. S.. (2002). Cell-specific effect of inerleukin-17 (IL-17) in inducible nitric oxide synthase (iNOS) activation.. in Clinical Immunology, 103(3).
https://hdl.handle.net/21.15107/rcub_ibiss_1794

Stošić-Grujičić S, Trajković VS, Miljković Đ, Stojanović ID, Maksimović-Ivanić D, Samardžić TS. Cell-specific effect of inerleukin-17 (IL-17) in inducible nitric oxide synthase (iNOS) activation.. in Clinical Immunology. 2002;103(3):null-S22.
https://hdl.handle.net/21.15107/rcub_ibiss_1794 .

Stošić-Grujičić, Stanislava, Trajković, Vladimir S, Miljković, Đorđe, Stojanović, Ivana D., Maksimović-Ivanić, Danijela, Samardžić, Tatjana S., "Cell-specific effect of inerleukin-17 (IL-17) in inducible nitric oxide synthase (iNOS) activation." in Clinical Immunology, 103, no. 3 (2002),
https://hdl.handle.net/21.15107/rcub_ibiss_1794 .

TY  - JOUR
AU  - Miljković, Đorđe
AU  - Samardžić, Tatjana
AU  - Stojanović, Ivana D.
AU  - Mostarica Stojković, Marija
AU  - Trajković, Vladimir
PY  - 2002
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5921
AB  - Free radical nitric oxide (NO), generated by inducible nitric oxide synthase (iNOS) in astrocytes and macrophages, has been implicated in CNS inflammatory disorders such as multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Mycophenolic acid (MPA), a selective inhibitor of inosine monophosphate dehydrogenase (IMPDH), inhibited interferon-gamam (IFN-gamma)  lipopolysaccharide (LPS)-induced NO production dose-dependently in astrocytes, but not in macrophages. The effect of MPA was not mediated through interference with IMPDHdependent synthesis of iNOS cofactor BH4 and subsequent suppression of iNOS enzymatic activity, as direct BH4 precursor sepiapterin failed to block the action of the drug. However, MPA markedly inhibited IFN-gamma  LPS-triggered astrocyte expression of mRNA for iNOS and its transcription factor IRF-1, while the expression of tumor necrosis factor- (TNF-) gene was not altered. The observed MPA suppression of NO release and iNOS and IRF-1 induction in astrocytes were efficiently prevented by exogenous guanosine, indicating that the drug acted through reduction of IMPDH dependent synthesis of guanosine nucleotides. This IRF-1-dependent inhibition of iNOS activation might be partly responsible for the protective effect of MPA in EAE, prompting investigation of its potential use in multiple sclerosis
PB  - Hoboken: Wiley
T2  - Glia
T1  - Mycophenolic acid downregulates inducible nitric oxide synthase induction in astrocytes
IS  - 3
VL  - 39
DO  - 10.1002/glia.10089
SP  - 247
EP  - 255
ER  - 

@article{
author = "Miljković, Đorđe and Samardžić, Tatjana and Stojanović, Ivana D. and Mostarica Stojković, Marija and Trajković, Vladimir",
year = "2002",
abstract = "Free radical nitric oxide (NO), generated by inducible nitric oxide synthase (iNOS) in astrocytes and macrophages, has been implicated in CNS inflammatory disorders such as multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Mycophenolic acid (MPA), a selective inhibitor of inosine monophosphate dehydrogenase (IMPDH), inhibited interferon-gamam (IFN-gamma)  lipopolysaccharide (LPS)-induced NO production dose-dependently in astrocytes, but not in macrophages. The effect of MPA was not mediated through interference with IMPDHdependent synthesis of iNOS cofactor BH4 and subsequent suppression of iNOS enzymatic activity, as direct BH4 precursor sepiapterin failed to block the action of the drug. However, MPA markedly inhibited IFN-gamma  LPS-triggered astrocyte expression of mRNA for iNOS and its transcription factor IRF-1, while the expression of tumor necrosis factor- (TNF-) gene was not altered. The observed MPA suppression of NO release and iNOS and IRF-1 induction in astrocytes were efficiently prevented by exogenous guanosine, indicating that the drug acted through reduction of IMPDH dependent synthesis of guanosine nucleotides. This IRF-1-dependent inhibition of iNOS activation might be partly responsible for the protective effect of MPA in EAE, prompting investigation of its potential use in multiple sclerosis",
publisher = "Hoboken: Wiley",
journal = "Glia",
title = "Mycophenolic acid downregulates inducible nitric oxide synthase induction in astrocytes",
number = "3",
volume = "39",
doi = "10.1002/glia.10089",
pages = "247-255"
}

Miljković, Đ., Samardžić, T., Stojanović, I. D., Mostarica Stojković, M.,& Trajković, V.. (2002). Mycophenolic acid downregulates inducible nitric oxide synthase induction in astrocytes. in Glia
Hoboken: Wiley., 39(3), 247-255.
https://doi.org/10.1002/glia.10089

Miljković Đ, Samardžić T, Stojanović ID, Mostarica Stojković M, Trajković V. Mycophenolic acid downregulates inducible nitric oxide synthase induction in astrocytes. in Glia. 2002;39(3):247-255.
doi:10.1002/glia.10089 .

Miljković, Đorđe, Samardžić, Tatjana, Stojanović, Ivana D., Mostarica Stojković, Marija, Trajković, Vladimir, "Mycophenolic acid downregulates inducible nitric oxide synthase induction in astrocytes" in Glia, 39, no. 3 (2002):247-255,
https://doi.org/10.1002/glia.10089 . .

TY  - JOUR
AU  - Samardžić, Tatjana S.
AU  - Stošić-Grujičić, Stanislava
AU  - Zogović, Nevena
AU  - Trajković, Vladimir S
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1817
AB  - The effects of tiazofurin (TR) on proliferation and cytokine-induced nitric oxide (NO) production in the L929 fibrosarcoma cell line and murine embryonic fibroblasts were investigated. Treatment with TR inhibited the growth of nonconfluent L929 cells in a dose-dependent manner. TR, at concentrations not affecting cell viability or proliferation, markedly decreased IFN-gamma + LPS-induced expression of inducible NO synthase (iNOS) mRNA and, subsequently. NO production in confluent L929 cultures. However, TR did not interfere with the IFN-gamma -triggered expression of mRNA for IRF-1, an important iNOS transcription factor, implying that TR interferes with some other intracellular pathway involved in iNOS induction triggered by IFN-gamma + LPS. In contrast to the results obtained in L929 cells, iNOS mRNA expression induced by IFN-gamma + LPS in murine embryonic fibroblasts was resistant to TR, indicating a tumor-selective action of this agent. (C) 2001 Elsevier Science B.V. All rights reserved.
T2  - International Immunopharmacology
T1  - Tumor cell-specific inhibition of inducible nitric oxide synthase activation by tiazofurin
IS  - 4
VL  - 1
EP  - 802
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1817
ER  - 

@article{
author = "Samardžić, Tatjana S. and Stošić-Grujičić, Stanislava and Zogović, Nevena and Trajković, Vladimir S",
year = "2001",
abstract = "The effects of tiazofurin (TR) on proliferation and cytokine-induced nitric oxide (NO) production in the L929 fibrosarcoma cell line and murine embryonic fibroblasts were investigated. Treatment with TR inhibited the growth of nonconfluent L929 cells in a dose-dependent manner. TR, at concentrations not affecting cell viability or proliferation, markedly decreased IFN-gamma + LPS-induced expression of inducible NO synthase (iNOS) mRNA and, subsequently. NO production in confluent L929 cultures. However, TR did not interfere with the IFN-gamma -triggered expression of mRNA for IRF-1, an important iNOS transcription factor, implying that TR interferes with some other intracellular pathway involved in iNOS induction triggered by IFN-gamma + LPS. In contrast to the results obtained in L929 cells, iNOS mRNA expression induced by IFN-gamma + LPS in murine embryonic fibroblasts was resistant to TR, indicating a tumor-selective action of this agent. (C) 2001 Elsevier Science B.V. All rights reserved.",
journal = "International Immunopharmacology",
title = "Tumor cell-specific inhibition of inducible nitric oxide synthase activation by tiazofurin",
number = "4",
volume = "1",
pages = "802",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1817"
}

Samardžić, T. S., Stošić-Grujičić, S., Zogović, N.,& Trajković, V. S.. (2001). Tumor cell-specific inhibition of inducible nitric oxide synthase activation by tiazofurin. in International Immunopharmacology, 1(4).
https://hdl.handle.net/21.15107/rcub_ibiss_1817

Samardžić TS, Stošić-Grujičić S, Zogović N, Trajković VS. Tumor cell-specific inhibition of inducible nitric oxide synthase activation by tiazofurin. in International Immunopharmacology. 2001;1(4):null-802.
https://hdl.handle.net/21.15107/rcub_ibiss_1817 .

Samardžić, Tatjana S., Stošić-Grujičić, Stanislava, Zogović, Nevena, Trajković, Vladimir S, "Tumor cell-specific inhibition of inducible nitric oxide synthase activation by tiazofurin" in International Immunopharmacology, 1, no. 4 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1817 .

TY  - JOUR
AU  - Drulović, Jelena
AU  - Dujmović, Irena
AU  - Mesaroš, Šarlota
AU  - Samardžić, Tatjana
AU  - Maksimović-Ivanić, Danijela
AU  - Stojsavljević, Nebojša
AU  - Lević, Zvonimir
AU  - Mostarica Stojković, Marija
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3842
AB  - A growing body of evidence implicates excessive generation of nitric oxide (NO) within the central nervous system (CNS) in multiple sclerosis (MS). The aim of our study is to analyse nitrite and nitrate as end products of NO in the cerebrospinal fluid (CSF) from MS patients and correlate the concentrations with clinicol characteristics of the disease. CSF nitrite and nitrate concentrations were measured after reduction of nitrate, by Griess reaction, in 105 MS potients, 27 patients with non-inflammatory neurological disorders (NIND) and 13 individuals without neurological disorder (Co). Mean CSF nitrite and nitrate concentrations were significantly higher in patients with MS and NIND compared with the Co patients (9.44 and 8.68, respectively, versus 6.85 microM; P=0.0001 and P=0.031, respectively). There was no significant correlation between CSF nitrite and nitrate concentrations and activity, phase, severity and duration of MS. Our data are in agreement with the results of previous studies which have demonstrated raised concentrations of CSF NO metabolites in MS patients, providing further evidence for NO involvement in MS. The lack of correlation between NO metabolites and disease activity speaks in favour of the possible dual role of NO, as both immunoregulatory and pro-inflammatory molecule, in the pathogenesis of MS.
PB  - Newbury Park: SAGE Publishing
T2  - Multiple Sclerosis Journal
T1  - Raised cerebrospinal fluid nitrite and nitrate levels in patients with multiple sclerosis: no correlation with disease activity
IS  - 1
VL  - 7
DO  - 10.1177/135245850100700104
SP  - 19
EP  - 22
ER  - 

@article{
author = "Drulović, Jelena and Dujmović, Irena and Mesaroš, Šarlota and Samardžić, Tatjana and Maksimović-Ivanić, Danijela and Stojsavljević, Nebojša and Lević, Zvonimir and Mostarica Stojković, Marija",
year = "2001",
abstract = "A growing body of evidence implicates excessive generation of nitric oxide (NO) within the central nervous system (CNS) in multiple sclerosis (MS). The aim of our study is to analyse nitrite and nitrate as end products of NO in the cerebrospinal fluid (CSF) from MS patients and correlate the concentrations with clinicol characteristics of the disease. CSF nitrite and nitrate concentrations were measured after reduction of nitrate, by Griess reaction, in 105 MS potients, 27 patients with non-inflammatory neurological disorders (NIND) and 13 individuals without neurological disorder (Co). Mean CSF nitrite and nitrate concentrations were significantly higher in patients with MS and NIND compared with the Co patients (9.44 and 8.68, respectively, versus 6.85 microM; P=0.0001 and P=0.031, respectively). There was no significant correlation between CSF nitrite and nitrate concentrations and activity, phase, severity and duration of MS. Our data are in agreement with the results of previous studies which have demonstrated raised concentrations of CSF NO metabolites in MS patients, providing further evidence for NO involvement in MS. The lack of correlation between NO metabolites and disease activity speaks in favour of the possible dual role of NO, as both immunoregulatory and pro-inflammatory molecule, in the pathogenesis of MS.",
publisher = "Newbury Park: SAGE Publishing",
journal = "Multiple Sclerosis Journal",
title = "Raised cerebrospinal fluid nitrite and nitrate levels in patients with multiple sclerosis: no correlation with disease activity",
number = "1",
volume = "7",
doi = "10.1177/135245850100700104",
pages = "19-22"
}

Drulović, J., Dujmović, I., Mesaroš, Š., Samardžić, T., Maksimović-Ivanić, D., Stojsavljević, N., Lević, Z.,& Mostarica Stojković, M.. (2001). Raised cerebrospinal fluid nitrite and nitrate levels in patients with multiple sclerosis: no correlation with disease activity. in Multiple Sclerosis Journal
Newbury Park: SAGE Publishing., 7(1), 19-22.
https://doi.org/10.1177/135245850100700104

Drulović J, Dujmović I, Mesaroš Š, Samardžić T, Maksimović-Ivanić D, Stojsavljević N, Lević Z, Mostarica Stojković M. Raised cerebrospinal fluid nitrite and nitrate levels in patients with multiple sclerosis: no correlation with disease activity. in Multiple Sclerosis Journal. 2001;7(1):19-22.
doi:10.1177/135245850100700104 .

Drulović, Jelena, Dujmović, Irena, Mesaroš, Šarlota, Samardžić, Tatjana, Maksimović-Ivanić, Danijela, Stojsavljević, Nebojša, Lević, Zvonimir, Mostarica Stojković, Marija, "Raised cerebrospinal fluid nitrite and nitrate levels in patients with multiple sclerosis: no correlation with disease activity" in Multiple Sclerosis Journal, 7, no. 1 (2001):19-22,
https://doi.org/10.1177/135245850100700104 . .

TY  - JOUR
AU  - Samardžić, Tatjana S.
AU  - Janković, V
AU  - Stošić-Grujičić, Stanislava
AU  - Popadić, Dusan M
AU  - Trajković, Vladimir S
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1815
AB  - The effect of phosphodiesterase-inhibiting anti-inflammatory drug pentoxifylline (PTX) on LPS-induced IL-18 synthesis and IL-18-mediated IFN-gamma -induction were investigated. In a dose-dependent manner PTX inhibited production of IL-18 in LPS-treated cultures of murine spleen cells and bone marrow-derived macrophages. Similarly, PTX treatment significantly reduced blood IL-18 levels and expression of spleen IL-18 mRNA in LPS-challenged mice. The inhibitory effect of PTX was specific for IL-18, since LPS-induced IL-12 p40 release was not suppressed either in splenocyte cultures or blood of LPS-injected animals. Synergistic induction of IFN-gamma by combined IL-12/IL-18 treatment was also inhibited by PTX in vitro and in vivo. Experiments with IL-12 pretreatment of splenocytes, followed by IL-18 stimulation, revealed that PTX suppressed both IL-12 and IL-18 signals responsible for IFN-gamma induction. These results suggest that interference with IL-18 synthesis and IFN-gamma -inducing activity might contribute to anti-inflammatory actions of PTX.
T2  - Clinical and Experimental Immunology
T1  - Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18
IS  - 2
VL  - 124
EP  - 281
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1815
ER  - 

@article{
author = "Samardžić, Tatjana S. and Janković, V and Stošić-Grujičić, Stanislava and Popadić, Dusan M and Trajković, Vladimir S",
year = "2001",
abstract = "The effect of phosphodiesterase-inhibiting anti-inflammatory drug pentoxifylline (PTX) on LPS-induced IL-18 synthesis and IL-18-mediated IFN-gamma -induction were investigated. In a dose-dependent manner PTX inhibited production of IL-18 in LPS-treated cultures of murine spleen cells and bone marrow-derived macrophages. Similarly, PTX treatment significantly reduced blood IL-18 levels and expression of spleen IL-18 mRNA in LPS-challenged mice. The inhibitory effect of PTX was specific for IL-18, since LPS-induced IL-12 p40 release was not suppressed either in splenocyte cultures or blood of LPS-injected animals. Synergistic induction of IFN-gamma by combined IL-12/IL-18 treatment was also inhibited by PTX in vitro and in vivo. Experiments with IL-12 pretreatment of splenocytes, followed by IL-18 stimulation, revealed that PTX suppressed both IL-12 and IL-18 signals responsible for IFN-gamma induction. These results suggest that interference with IL-18 synthesis and IFN-gamma -inducing activity might contribute to anti-inflammatory actions of PTX.",
journal = "Clinical and Experimental Immunology",
title = "Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18",
number = "2",
volume = "124",
pages = "281",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1815"
}

Samardžić, T. S., Janković, V., Stošić-Grujičić, S., Popadić, D. M.,& Trajković, V. S.. (2001). Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18. in Clinical and Experimental Immunology, 124(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1815

Samardžić TS, Janković V, Stošić-Grujičić S, Popadić DM, Trajković VS. Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18. in Clinical and Experimental Immunology. 2001;124(2):null-281.
https://hdl.handle.net/21.15107/rcub_ibiss_1815 .

Samardžić, Tatjana S., Janković, V, Stošić-Grujičić, Stanislava, Popadić, Dusan M, Trajković, Vladimir S, "Pentoxifylline inhibits the synthesis and IFN-gamma-inducing activity of IL-18" in Clinical and Experimental Immunology, 124, no. 2 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1815 .

TY  - JOUR
AU  - Stepanović, Srđan
AU  - Vuković, Dragana
AU  - Trajković, Vladimir S
AU  - Samardžić, Tatjana S.
AU  - Cupić, Maja D
AU  - Svabić-Vlahović, Milena
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1814
AB  - Staplylococcus sciuri is an opportunistic pathogen of controversial clinical significance. The factors that contribute to colonization and/or infection caused by this bacterium have not been studied intensively so far. The present research was carried out in order to study the presence of potential virulence factors in 121 human and animal isolates of this bacterium. Isolates were examined for biofilm formation, hemagglutination, presence of clumping factor, production of spreading factors and exotoxins, cytotoxicity and capacity to stimulate nitric oxide production. The results showed that S. sciuri is highly capable of biofilm production, that it displays strong proteolytic and DNase activities, produces hemolysins and stimulates nitric oxide production by rat macrophages. Although the present study showed existence of a wide spectrum of possible virulence determinants of S. sciuri. their exact contribution to virulence of this bacterium in vivo remains to be determined. (C) 2001 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.
T2  - Fems Microbiology Letters
T1  - Possible virulence factors of Staphylococcus sciuri
IS  - 1
VL  - 199
EP  - 53
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1814
ER  - 

@article{
author = "Stepanović, Srđan and Vuković, Dragana and Trajković, Vladimir S and Samardžić, Tatjana S. and Cupić, Maja D and Svabić-Vlahović, Milena",
year = "2001",
abstract = "Staplylococcus sciuri is an opportunistic pathogen of controversial clinical significance. The factors that contribute to colonization and/or infection caused by this bacterium have not been studied intensively so far. The present research was carried out in order to study the presence of potential virulence factors in 121 human and animal isolates of this bacterium. Isolates were examined for biofilm formation, hemagglutination, presence of clumping factor, production of spreading factors and exotoxins, cytotoxicity and capacity to stimulate nitric oxide production. The results showed that S. sciuri is highly capable of biofilm production, that it displays strong proteolytic and DNase activities, produces hemolysins and stimulates nitric oxide production by rat macrophages. Although the present study showed existence of a wide spectrum of possible virulence determinants of S. sciuri. their exact contribution to virulence of this bacterium in vivo remains to be determined. (C) 2001 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.",
journal = "Fems Microbiology Letters",
title = "Possible virulence factors of Staphylococcus sciuri",
number = "1",
volume = "199",
pages = "53",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1814"
}

Stepanović, S., Vuković, D., Trajković, V. S., Samardžić, T. S., Cupić, M. D.,& Svabić-Vlahović, M.. (2001). Possible virulence factors of Staphylococcus sciuri. in Fems Microbiology Letters, 199(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1814

Stepanović S, Vuković D, Trajković VS, Samardžić TS, Cupić MD, Svabić-Vlahović M. Possible virulence factors of Staphylococcus sciuri. in Fems Microbiology Letters. 2001;199(1):null-53.
https://hdl.handle.net/21.15107/rcub_ibiss_1814 .

Stepanović, Srđan, Vuković, Dragana, Trajković, Vladimir S, Samardžić, Tatjana S., Cupić, Maja D, Svabić-Vlahović, Milena, "Possible virulence factors of Staphylococcus sciuri" in Fems Microbiology Letters, 199, no. 1 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1814 .

TY  - JOUR
AU  - Stošić-Grujičić, Stanislava
AU  - Maksimović-Ivanić, Danijela
AU  - Badovinac, Vladimir
AU  - Samardžić, Tatjana S.
AU  - Trajković, Vladimir S
AU  - Lukić, Miodrag L
AU  - Mostarica-Stojković, Marija B
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1821
AB  - We have shown recently that xanthine derivative pentoxifylline (PTX) downregulates an inflammatory autoimmune process triggered in genetically susceptible Dark Agouti rats by multiple low doses of streptozotocin (MLD-SZ, 20 mg/kg/day ip for 5 days). We studied the cellular and molecular consequences of PTX treatment during MLD-SZ-induced diabetes with special emphasis on local vs. systemic production of inflammatory mediators. Administration of PTX (200 mg/kg/day for 10 days) during induction of the disease reduced clinical signs of diabetes and protected rats from development of destructive intrainsulitis. Pentoxifylline did not affect diabetogenic effect of single high dose of SZ (100 mg/kg SZ). Ex vivo analysis of the islets of Langerhans performed in early disease development revealed that PTX downregulates production of proinflammatory cytokines IFN-gamma and TNF, as well as inducible nitric oxide synthase (iNOS) expression and NO production. In addition, PTX treatment suppressed splenocyte autoreactivity, as well as the frequency of cells expressing IL-2R and MHC class II antigens. There was no evidence of any changes in proportion of ICAM-1 and LFA-1 expressing splenocytes in comparison to control MLD-SZ-treated animals. In contrast to suppressed intraislet production, high peripheral expression of both iNOS mRNA and NO was found in MLD-SZ rats treated with PTX. Taken together, the data indicate that the effect on both systemic and intra-islet production of NO, suppression of autoreactive cell activation and of local type 1 cytokine release may contribute to the therapeutic benefit achieved by PTX in the rat. (C) 2001 Academic Press.
T2  - Journal of Autoimmunity
T1  - Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production
IS  - 1
VL  - 16
EP  - 58
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1821
ER  - 

@article{
author = "Stošić-Grujičić, Stanislava and Maksimović-Ivanić, Danijela and Badovinac, Vladimir and Samardžić, Tatjana S. and Trajković, Vladimir S and Lukić, Miodrag L and Mostarica-Stojković, Marija B",
year = "2001",
abstract = "We have shown recently that xanthine derivative pentoxifylline (PTX) downregulates an inflammatory autoimmune process triggered in genetically susceptible Dark Agouti rats by multiple low doses of streptozotocin (MLD-SZ, 20 mg/kg/day ip for 5 days). We studied the cellular and molecular consequences of PTX treatment during MLD-SZ-induced diabetes with special emphasis on local vs. systemic production of inflammatory mediators. Administration of PTX (200 mg/kg/day for 10 days) during induction of the disease reduced clinical signs of diabetes and protected rats from development of destructive intrainsulitis. Pentoxifylline did not affect diabetogenic effect of single high dose of SZ (100 mg/kg SZ). Ex vivo analysis of the islets of Langerhans performed in early disease development revealed that PTX downregulates production of proinflammatory cytokines IFN-gamma and TNF, as well as inducible nitric oxide synthase (iNOS) expression and NO production. In addition, PTX treatment suppressed splenocyte autoreactivity, as well as the frequency of cells expressing IL-2R and MHC class II antigens. There was no evidence of any changes in proportion of ICAM-1 and LFA-1 expressing splenocytes in comparison to control MLD-SZ-treated animals. In contrast to suppressed intraislet production, high peripheral expression of both iNOS mRNA and NO was found in MLD-SZ rats treated with PTX. Taken together, the data indicate that the effect on both systemic and intra-islet production of NO, suppression of autoreactive cell activation and of local type 1 cytokine release may contribute to the therapeutic benefit achieved by PTX in the rat. (C) 2001 Academic Press.",
journal = "Journal of Autoimmunity",
title = "Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production",
number = "1",
volume = "16",
pages = "58",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1821"
}

Stošić-Grujičić, S., Maksimović-Ivanić, D., Badovinac, V., Samardžić, T. S., Trajković, V. S., Lukić, M. L.,& Mostarica-Stojković, M. B.. (2001). Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production. in Journal of Autoimmunity, 16(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1821

Stošić-Grujičić S, Maksimović-Ivanić D, Badovinac V, Samardžić TS, Trajković VS, Lukić ML, Mostarica-Stojković MB. Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production. in Journal of Autoimmunity. 2001;16(1):null-58.
https://hdl.handle.net/21.15107/rcub_ibiss_1821 .

Stošić-Grujičić, Stanislava, Maksimović-Ivanić, Danijela, Badovinac, Vladimir, Samardžić, Tatjana S., Trajković, Vladimir S, Lukić, Miodrag L, Mostarica-Stojković, Marija B, "Antidiabetogenic effect of pentoxifylline is associated with systemic and target tissue modulation of cytokines and nitric oxide production" in Journal of Autoimmunity, 16, no. 1 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1821 .

TY  - JOUR
AU  - Samardžić, Tatjana S.
AU  - Janković, V
AU  - Stošić-Grujičić, Stanislava
AU  - Trajković, Vladimir S
PY  - 2001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1820
AB  - The role of transcription factor STAT1 in production of pro-inflammatory mediators nitric oxide (NO) and IL-6 was examined in murine embryonic fibroblasts. While cells from wild-type animals released large amounts of NO after stimulation with IFN-gamma in combination with LPS, TNF-alpha or IL-1, their STAT1-deficient counterparts failed to synthesise detectable levels of this free radical gas. Inability of STAT1(-/-) fibroblasts to produce NO was accompanied by complete absence of mRNA for iNOS and its transcription factor IRF-1, both readily upregulated in wild-type cells. However, treatment with cytokines (IFN-gamma, TNF-alpha, IL-1, IL-17) significantly increased IL-6 generation in STAT1-deficient fibroblasts. These results indicate that STAT1 activation and subsequent IRF-1 transcription are required for induction of iNOS, but not IL-6 in murine fibroblasts. (C) 2001 Academic Press.
T2  - Cytokine
T1  - STAT1 is required for iNOS activation, but not IL-6 production in murine fibroblasts
IS  - 3
VL  - 13
EP  - 182
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1820
ER  - 

@article{
author = "Samardžić, Tatjana S. and Janković, V and Stošić-Grujičić, Stanislava and Trajković, Vladimir S",
year = "2001",
abstract = "The role of transcription factor STAT1 in production of pro-inflammatory mediators nitric oxide (NO) and IL-6 was examined in murine embryonic fibroblasts. While cells from wild-type animals released large amounts of NO after stimulation with IFN-gamma in combination with LPS, TNF-alpha or IL-1, their STAT1-deficient counterparts failed to synthesise detectable levels of this free radical gas. Inability of STAT1(-/-) fibroblasts to produce NO was accompanied by complete absence of mRNA for iNOS and its transcription factor IRF-1, both readily upregulated in wild-type cells. However, treatment with cytokines (IFN-gamma, TNF-alpha, IL-1, IL-17) significantly increased IL-6 generation in STAT1-deficient fibroblasts. These results indicate that STAT1 activation and subsequent IRF-1 transcription are required for induction of iNOS, but not IL-6 in murine fibroblasts. (C) 2001 Academic Press.",
journal = "Cytokine",
title = "STAT1 is required for iNOS activation, but not IL-6 production in murine fibroblasts",
number = "3",
volume = "13",
pages = "182",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1820"
}

Samardžić, T. S., Janković, V., Stošić-Grujičić, S.,& Trajković, V. S.. (2001). STAT1 is required for iNOS activation, but not IL-6 production in murine fibroblasts. in Cytokine, 13(3).
https://hdl.handle.net/21.15107/rcub_ibiss_1820

Samardžić TS, Janković V, Stošić-Grujičić S, Trajković VS. STAT1 is required for iNOS activation, but not IL-6 production in murine fibroblasts. in Cytokine. 2001;13(3):null-182.
https://hdl.handle.net/21.15107/rcub_ibiss_1820 .

Samardžić, Tatjana S., Janković, V, Stošić-Grujičić, Stanislava, Trajković, Vladimir S, "STAT1 is required for iNOS activation, but not IL-6 production in murine fibroblasts" in Cytokine, 13, no. 3 (2001),
https://hdl.handle.net/21.15107/rcub_ibiss_1820 .

TY  - JOUR
AU  - Janković, V
AU  - Samardžić, Tatjana S.
AU  - Stošić-Grujičić, Stanislava
AU  - Popadić, Dusan M
AU  - Trajković, Vladimir S
PY  - 2000
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1834
AB  - The influence of a novel immunomodulating drug, leflunomide, on iNOS-dependent nitric oxide (NO) production in rodent macrophages and fibroblasts was investigated. Leflunomide's active metabolite A77 1726 caused a dose-dependent decrease of NO production in IFN-gamma-treated L929 fibroblasts. The observed effect was cell-specific, as well as stimulus-specific, since A77 1726 did not affect NO production in IFN-gamma-stimulated murine peritoneal macrophages or db-cAMP-treated L929 cells. A77 1726 reduced expression of IFN-gamma-induced iNOS and IRF-1 mRNA in L929 cells, while iNOS enzymatic activity remained unchanged. Specific inhibitor of MAP kinase kinase (MEK), PD98059, but not unselective protein kinase inhibitor genistein, completely mimicked cell-type-specific and stimulus-specific NO-inhibitory action of leflunomide. Therefore, the recently described inhibition of MEK/MAP pathway by leflunomide could present a possible mechanism for its suppression of iNOS activation in L929 fibroblasts. Finally, a similar inhibitory effect of A77 1726 on both NO production and iNOS mRNA expression was observed also in IFN-gamma + LPS-activated murine and rat primary fibroblasts. (C) 2000 Academic Press.
T2  - Cellular Immunology
T1  - Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide
IS  - 2
VL  - 199
EP  - 80
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1834
ER  - 

@article{
author = "Janković, V and Samardžić, Tatjana S. and Stošić-Grujičić, Stanislava and Popadić, Dusan M and Trajković, Vladimir S",
year = "2000",
abstract = "The influence of a novel immunomodulating drug, leflunomide, on iNOS-dependent nitric oxide (NO) production in rodent macrophages and fibroblasts was investigated. Leflunomide's active metabolite A77 1726 caused a dose-dependent decrease of NO production in IFN-gamma-treated L929 fibroblasts. The observed effect was cell-specific, as well as stimulus-specific, since A77 1726 did not affect NO production in IFN-gamma-stimulated murine peritoneal macrophages or db-cAMP-treated L929 cells. A77 1726 reduced expression of IFN-gamma-induced iNOS and IRF-1 mRNA in L929 cells, while iNOS enzymatic activity remained unchanged. Specific inhibitor of MAP kinase kinase (MEK), PD98059, but not unselective protein kinase inhibitor genistein, completely mimicked cell-type-specific and stimulus-specific NO-inhibitory action of leflunomide. Therefore, the recently described inhibition of MEK/MAP pathway by leflunomide could present a possible mechanism for its suppression of iNOS activation in L929 fibroblasts. Finally, a similar inhibitory effect of A77 1726 on both NO production and iNOS mRNA expression was observed also in IFN-gamma + LPS-activated murine and rat primary fibroblasts. (C) 2000 Academic Press.",
journal = "Cellular Immunology",
title = "Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide",
number = "2",
volume = "199",
pages = "80",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1834"
}

Janković, V., Samardžić, T. S., Stošić-Grujičić, S., Popadić, D. M.,& Trajković, V. S.. (2000). Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide. in Cellular Immunology, 199(2).
https://hdl.handle.net/21.15107/rcub_ibiss_1834

Janković V, Samardžić TS, Stošić-Grujičić S, Popadić DM, Trajković VS. Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide. in Cellular Immunology. 2000;199(2):null-80.
https://hdl.handle.net/21.15107/rcub_ibiss_1834 .

Janković, V, Samardžić, Tatjana S., Stošić-Grujičić, Stanislava, Popadić, Dusan M, Trajković, Vladimir S, "Cell-specific inhibition of inducible nitric oxide synthase activation by leflunomide" in Cellular Immunology, 199, no. 2 (2000),
https://hdl.handle.net/21.15107/rcub_ibiss_1834 .

TY  - JOUR
AU  - Trajković, Vladimir S
AU  - Stepanović, Srđan
AU  - Samardžić, Tatjana S.
AU  - Janković, V
AU  - Badovinac, Vladimir
AU  - Mostarica-Stojković, Marija B
PY  - 2000
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1833
AB  - The effect of Cryptococcus neoformans on the accumulation of nitrite, an indicator of nitric oxide (NO) synthesis, was investigated in cytokine (interferon-gamma [IFN-gamma] and interleukin [IL]-1)-stimulated cultures of rat peritoneal macrophages and C6 astrocytoma cells. Cytokine-induced nitrite generation in cultures of both cell types was inhibited in a dose-dependent manner by live C. neoformans, but not by heat-killed cryptococcal cells or conditioned medium from yeast cultures. C. neoformans-mediated reduction of nitrite formation coincided with impairment of NO-dependent macrophage tumoricidal activity. Cytokine-triggered induction of inducible NO synthase (iNOS) was unaffected in C6 cells, and only marginally reduced in macrophages. When cells were pretreated with cytokines for 24 h to induce iNOS, and any further induction was prevented by inhibition of protein synthesis, C. neoformans was still able to reduce nitrite accumulation in cultures of both cell types. Finally, live C. neoformans, but not heat-killed yeast cells or yeast culture supernatant, significantly reduced nitrite production in a culture solution of NO-releasing compound S-nitrosoglutathione (GSNO). Thus, it appears that cryptococcal reduction of nitrite formation in macrophage and C6 cultures was caused by the consumption of NO by some yeast molecule, rather than by the inhibition of cellular NO synthesis.
T2  - Scandinavian Journal of Immunology
T1  - Cryptococcus neoformans neutralizes macrophage and astrocyte derived nitric oxide without interfering with inducible nitric oxide synthase induction or catalytic activity - Possible involvement of nitric oxide consumption
IS  - 4
VL  - 51
EP  - 391
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1833
ER  - 

@article{
author = "Trajković, Vladimir S and Stepanović, Srđan and Samardžić, Tatjana S. and Janković, V and Badovinac, Vladimir and Mostarica-Stojković, Marija B",
year = "2000",
abstract = "The effect of Cryptococcus neoformans on the accumulation of nitrite, an indicator of nitric oxide (NO) synthesis, was investigated in cytokine (interferon-gamma [IFN-gamma] and interleukin [IL]-1)-stimulated cultures of rat peritoneal macrophages and C6 astrocytoma cells. Cytokine-induced nitrite generation in cultures of both cell types was inhibited in a dose-dependent manner by live C. neoformans, but not by heat-killed cryptococcal cells or conditioned medium from yeast cultures. C. neoformans-mediated reduction of nitrite formation coincided with impairment of NO-dependent macrophage tumoricidal activity. Cytokine-triggered induction of inducible NO synthase (iNOS) was unaffected in C6 cells, and only marginally reduced in macrophages. When cells were pretreated with cytokines for 24 h to induce iNOS, and any further induction was prevented by inhibition of protein synthesis, C. neoformans was still able to reduce nitrite accumulation in cultures of both cell types. Finally, live C. neoformans, but not heat-killed yeast cells or yeast culture supernatant, significantly reduced nitrite production in a culture solution of NO-releasing compound S-nitrosoglutathione (GSNO). Thus, it appears that cryptococcal reduction of nitrite formation in macrophage and C6 cultures was caused by the consumption of NO by some yeast molecule, rather than by the inhibition of cellular NO synthesis.",
journal = "Scandinavian Journal of Immunology",
title = "Cryptococcus neoformans neutralizes macrophage and astrocyte derived nitric oxide without interfering with inducible nitric oxide synthase induction or catalytic activity - Possible involvement of nitric oxide consumption",
number = "4",
volume = "51",
pages = "391",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1833"
}

Trajković, V. S., Stepanović, S., Samardžić, T. S., Janković, V., Badovinac, V.,& Mostarica-Stojković, M. B.. (2000). Cryptococcus neoformans neutralizes macrophage and astrocyte derived nitric oxide without interfering with inducible nitric oxide synthase induction or catalytic activity - Possible involvement of nitric oxide consumption. in Scandinavian Journal of Immunology, 51(4).
https://hdl.handle.net/21.15107/rcub_ibiss_1833

Trajković VS, Stepanović S, Samardžić TS, Janković V, Badovinac V, Mostarica-Stojković MB. Cryptococcus neoformans neutralizes macrophage and astrocyte derived nitric oxide without interfering with inducible nitric oxide synthase induction or catalytic activity - Possible involvement of nitric oxide consumption. in Scandinavian Journal of Immunology. 2000;51(4):null-391.
https://hdl.handle.net/21.15107/rcub_ibiss_1833 .

Trajković, Vladimir S, Stepanović, Srđan, Samardžić, Tatjana S., Janković, V, Badovinac, Vladimir, Mostarica-Stojković, Marija B, "Cryptococcus neoformans neutralizes macrophage and astrocyte derived nitric oxide without interfering with inducible nitric oxide synthase induction or catalytic activity - Possible involvement of nitric oxide consumption" in Scandinavian Journal of Immunology, 51, no. 4 (2000),
https://hdl.handle.net/21.15107/rcub_ibiss_1833 .