TY  - JOUR
AU  - Stevanović, Darko M
AU  - Starčević, Vesna P.
AU  - Vilimanović, Uros
AU  - Nesić, Dejan M
AU  - Vučićević, Ljubica
AU  - Misirkić Marjanović, Maja
AU  - Janjetović, Kristina
AU  - Savić, Emina
AU  - Popadić, Dusan M
AU  - Sudar, Emina M
AU  - Micić, Dragan D
AU  - Sumarac-Dumanović, Mirjana S
AU  - Trajković, Vladimir S
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1238
AB  - We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Brain Behavior and Immunity
T1  - Immunomodulatory actions of central ghrelin in diet-induced energy imbalance
IS  - 1
VL  - 26
EP  - 158
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1238
ER  - 

@article{
author = "Stevanović, Darko M and Starčević, Vesna P. and Vilimanović, Uros and Nesić, Dejan M and Vučićević, Ljubica and Misirkić Marjanović, Maja and Janjetović, Kristina and Savić, Emina and Popadić, Dusan M and Sudar, Emina M and Micić, Dragan D and Sumarac-Dumanović, Mirjana S and Trajković, Vladimir S",
year = "2012",
abstract = "We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Brain Behavior and Immunity",
title = "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance",
number = "1",
volume = "26",
pages = "158",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1238"
}

Stevanović, D. M., Starčević, V. P., Vilimanović, U., Nesić, D. M., Vučićević, L., Misirkić Marjanović, M., Janjetović, K., Savić, E., Popadić, D. M., Sudar, E. M., Micić, D. D., Sumarac-Dumanović, M. S.,& Trajković, V. S.. (2012). Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity, 26(1).
https://hdl.handle.net/21.15107/rcub_ibiss_1238

Stevanović DM, Starčević VP, Vilimanović U, Nesić DM, Vučićević L, Misirkić Marjanović M, Janjetović K, Savić E, Popadić DM, Sudar EM, Micić DD, Sumarac-Dumanović MS, Trajković VS. Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity. 2012;26(1):null-158.
https://hdl.handle.net/21.15107/rcub_ibiss_1238 .

Stevanović, Darko M, Starčević, Vesna P., Vilimanović, Uros, Nesić, Dejan M, Vučićević, Ljubica, Misirkić Marjanović, Maja, Janjetović, Kristina, Savić, Emina, Popadić, Dusan M, Sudar, Emina M, Micić, Dragan D, Sumarac-Dumanović, Mirjana S, Trajković, Vladimir S, "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance" in Brain Behavior and Immunity, 26, no. 1 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1238 .

TY  - JOUR
AU  - Marković, Milos
AU  - Miljković, Đorđe
AU  - Momčilović, Miljana
AU  - Popadić, Dusan M
AU  - Miljković, Zeljka
AU  - Savić, Emina
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija B
PY  - 2009
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1129
AB  - Albino Oxford (AO) rats are resistant to induction of experimental autoimmune encephalomyelitis (EAE), in contrast to susceptible Dark Agouti (DA) rats. We have previously shown that draining lymph node cells (DLNC) obtained from immunized DA rats before the onset of the clinical disease produced more interferon (IFN)-gamma and interleukin (IL)-17 (signature cytokines of T(H)1 and T(H)17 responses, respectively) compared to DLNC from AO rats. In this study, we extend our analysis to entire induction phase of EAE with the emphasis on the T(H)1 and T(H)17-inducing cytokines. As a result, we show that throughout the inductive phase of the disease DLNC of DA rats, not only expressed higher levels of IFN-gamma and IL-17, but also of T(H)1-inducing cytokine-IL-12. As for T(H)17-inducing cytokines, DLNC of DA rats expressed more mRNA for p19, specific subunit of IL-23, but the expression of transforming growth factor (TGF)-beta in both strains was similar. Interestingly, the analysis of IL-6 expression revealed striking difference: while all DA DLNC were positive for IL-6 mRNA, cells from none of AO rats expressed detectable levels of mRNA for this cytokine. Taken together, our data suggest that the differential regulation of production of T(H)1 and T(H)17 cytokines, and IL-6 in particular, during the induction phase of disease could be responsible for the discrepancy in susceptibility to EAE between these two rat strains. (C) 2009 Elsevier Ltd. All rights reserved.
T2  - Molecular Immunology
T1  - Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles
IS  - 1
VL  - 47
SP  - 243
EP  - 146
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1129
ER  - 

@article{
author = "Marković, Milos and Miljković, Đorđe and Momčilović, Miljana and Popadić, Dusan M and Miljković, Zeljka and Savić, Emina and Ramić, Zorica D. and Mostarica-Stojković, Marija B",
year = "2009",
abstract = "Albino Oxford (AO) rats are resistant to induction of experimental autoimmune encephalomyelitis (EAE), in contrast to susceptible Dark Agouti (DA) rats. We have previously shown that draining lymph node cells (DLNC) obtained from immunized DA rats before the onset of the clinical disease produced more interferon (IFN)-gamma and interleukin (IL)-17 (signature cytokines of T(H)1 and T(H)17 responses, respectively) compared to DLNC from AO rats. In this study, we extend our analysis to entire induction phase of EAE with the emphasis on the T(H)1 and T(H)17-inducing cytokines. As a result, we show that throughout the inductive phase of the disease DLNC of DA rats, not only expressed higher levels of IFN-gamma and IL-17, but also of T(H)1-inducing cytokine-IL-12. As for T(H)17-inducing cytokines, DLNC of DA rats expressed more mRNA for p19, specific subunit of IL-23, but the expression of transforming growth factor (TGF)-beta in both strains was similar. Interestingly, the analysis of IL-6 expression revealed striking difference: while all DA DLNC were positive for IL-6 mRNA, cells from none of AO rats expressed detectable levels of mRNA for this cytokine. Taken together, our data suggest that the differential regulation of production of T(H)1 and T(H)17 cytokines, and IL-6 in particular, during the induction phase of disease could be responsible for the discrepancy in susceptibility to EAE between these two rat strains. (C) 2009 Elsevier Ltd. All rights reserved.",
journal = "Molecular Immunology",
title = "Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles",
number = "1",
volume = "47",
pages = "243-146",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1129"
}

Marković, M., Miljković, Đ., Momčilović, M., Popadić, D. M., Miljković, Z., Savić, E., Ramić, Z. D.,& Mostarica-Stojković, M. B.. (2009). Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles. in Molecular Immunology, 47(1), 243-146.
https://hdl.handle.net/21.15107/rcub_ibiss_1129

Marković M, Miljković Đ, Momčilović M, Popadić DM, Miljković Z, Savić E, Ramić ZD, Mostarica-Stojković MB. Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles. in Molecular Immunology. 2009;47(1):243-146.
https://hdl.handle.net/21.15107/rcub_ibiss_1129 .

Marković, Milos, Miljković, Đorđe, Momčilović, Miljana, Popadić, Dusan M, Miljković, Zeljka, Savić, Emina, Ramić, Zorica D., Mostarica-Stojković, Marija B, "Strain difference in susceptibility to experimental autoimmune encephalomyelitis in rats correlates with T(H)1 and T(H)17-inducing cytokine profiles" in Molecular Immunology, 47, no. 1 (2009):243-146,
https://hdl.handle.net/21.15107/rcub_ibiss_1129 .

TY  - JOUR
AU  - Momčilović, Miljana
AU  - Miljković, Zeljka
AU  - Popadić, Dusan M
AU  - Marković, Milos
AU  - Savić, Emina
AU  - Ramić, Zorica D.
AU  - Miljković, Đorđe
AU  - Mostarica-Stojković, Marija B
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1519
AB  - Background: Interleukin-17 (IL-17)-producing cells are increasingly considered to be the major pathogenic population in various autoimmune disorders. The effects of glucocorticoids, widely used as therapeutics for inflammatory and autoimmune disorders, on IL-17 generation have not been thoroughly investigated so far. Therefore, we have explored the influence of methylprednisolone (MP) on IL-17 expression in rat lymphocytes, and compared it to the effect of the drug on interferon (IFN)-gamma. Results: Production of IL-17 in mitogen-stimulated lymph node cells (LNC) from non-treated rats, as well as in myelin basic protein (MBP)-stimulated draining LNC from rats immunized with spinal cord homogenate and complete Freund's adjuvant was significantly reduced by MP. The reduction was dose-dependent, sustained through the follow-up period of 48 hours, and was not achieved through anti-proliferative effect. Additionally, MP inhibited IL-17 production in purified T cells as well, but to less extent than in LNC. In its influence on IL-17 production MP inhibited Ror-gamma T transcription factor expression, as well as Jun phosphorylation, but not ERK or p38 activation in mitogen-stimulated LNC. Importantly, MP collaborated with IFN-gamma in inhibiting IL-17 generation in LNC. Conclusion: The observed difference in the effect of MP on IL-17 and IFN-gamma could be important for the understanding of the variability in the efficiency of glucocorticoids in the treatment of autoimmune diseases.
T2  - Bmc Immunology
T1  - Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells
IS  - null
VL  - 9
EP  - na
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1519
ER  - 

@article{
author = "Momčilović, Miljana and Miljković, Zeljka and Popadić, Dusan M and Marković, Milos and Savić, Emina and Ramić, Zorica D. and Miljković, Đorđe and Mostarica-Stojković, Marija B",
year = "2008",
abstract = "Background: Interleukin-17 (IL-17)-producing cells are increasingly considered to be the major pathogenic population in various autoimmune disorders. The effects of glucocorticoids, widely used as therapeutics for inflammatory and autoimmune disorders, on IL-17 generation have not been thoroughly investigated so far. Therefore, we have explored the influence of methylprednisolone (MP) on IL-17 expression in rat lymphocytes, and compared it to the effect of the drug on interferon (IFN)-gamma. Results: Production of IL-17 in mitogen-stimulated lymph node cells (LNC) from non-treated rats, as well as in myelin basic protein (MBP)-stimulated draining LNC from rats immunized with spinal cord homogenate and complete Freund's adjuvant was significantly reduced by MP. The reduction was dose-dependent, sustained through the follow-up period of 48 hours, and was not achieved through anti-proliferative effect. Additionally, MP inhibited IL-17 production in purified T cells as well, but to less extent than in LNC. In its influence on IL-17 production MP inhibited Ror-gamma T transcription factor expression, as well as Jun phosphorylation, but not ERK or p38 activation in mitogen-stimulated LNC. Importantly, MP collaborated with IFN-gamma in inhibiting IL-17 generation in LNC. Conclusion: The observed difference in the effect of MP on IL-17 and IFN-gamma could be important for the understanding of the variability in the efficiency of glucocorticoids in the treatment of autoimmune diseases.",
journal = "Bmc Immunology",
title = "Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells",
number = "null",
volume = "9",
pages = "na",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1519"
}

Momčilović, M., Miljković, Z., Popadić, D. M., Marković, M., Savić, E., Ramić, Z. D., Miljković, Đ.,& Mostarica-Stojković, M. B.. (2008). Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells. in Bmc Immunology, 9(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1519

Momčilović M, Miljković Z, Popadić DM, Marković M, Savić E, Ramić ZD, Miljković Đ, Mostarica-Stojković MB. Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells. in Bmc Immunology. 2008;9(null):null-na.
https://hdl.handle.net/21.15107/rcub_ibiss_1519 .

Momčilović, Miljana, Miljković, Zeljka, Popadić, Dusan M, Marković, Milos, Savić, Emina, Ramić, Zorica D., Miljković, Đorđe, Mostarica-Stojković, Marija B, "Methylprednisolone inhibits interleukin-17 and interferon-gamma expression by both naive and primed T cells" in Bmc Immunology, 9, no. null (2008),
https://hdl.handle.net/21.15107/rcub_ibiss_1519 .