Dinić, Miroslav

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694765e7-3e5e-47d9-bc5f-96867531c092
  • Dinić, Miroslav (2)
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Author's Bibliography

Polyphenols as inhibitors of antibiotic resistant bacteria - Mechanisms underlying rutin interference with bacterial virulence

Ivanov, Marija; Novović, Katarina; Malešević, Milka; Dinić, Miroslav; Stojković, Dejan; Jovčić, Branko; Soković, Marina

(Basel: MDPI, 2022)

TY  - JOUR
AU  - Ivanov, Marija
AU  - Novović, Katarina
AU  - Malešević, Milka
AU  - Dinić, Miroslav
AU  - Stojković, Dejan
AU  - Jovčić, Branko
AU  - Soković, Marina
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5558
AB  - The rising incidence of antibiotic resistant microorganisms urges novel antimicrobials development with polyphenols as appealing potential therapeutics. We aimed to reveal the most promising polyphenols among hesperetin, hesperidin, naringenin, naringin, taxifolin, rutin, isoquercitrin, morin, chlorogenic acid, ferulic acid, p-coumaric acid, and gallic acid based on antimicrobial capacity, antibiofilm potential, and lack of cytotoxicity towards HaCaT, and to further test its antivirulence mechanisms. Although the majority of studied polyphenols were able to inhibit bacterial growth and biofilm formation, the most promising activities were observed for rutin. Further investigation proved rutin's ability to prevent/eradicate Pseudomonas aeruginosa and MRSA urinary catheter biofilms. Besides reduction of biofilm biomass, rutin antibiofilm mechanisms included reduction of cell viability, exopolysaccharide, and extracellular DNA levels. Moderate reduction of bacterial adhesion to human keratinocytes upon treatment was observed. Rutin antivirulence mechanisms included an impact on P. aeruginosa protease, pyocyanin, rhamnolipid, and elastase production and the downregulation of the lasI, lasR, rhlI, rhlR, pqsA and mvfR genes. Rutin also interfered with membrane permeability. Polyphenols could repress antibiotic resistant bacteria. Rutin has shown wide antimicrobial and antibiofilm capacity employing a range of mechanisms that might be used for the development of novel antimicrobials.
PB  - Basel: MDPI
T2  - Pharmaceuticals
T1  - Polyphenols as inhibitors of antibiotic resistant bacteria - Mechanisms underlying rutin interference with bacterial virulence
IS  - 3
VL  - 15
DO  - 10.3390/ph15030385
SP  - 385
ER  - 
@article{
author = "Ivanov, Marija and Novović, Katarina and Malešević, Milka and Dinić, Miroslav and Stojković, Dejan and Jovčić, Branko and Soković, Marina",
year = "2022",
abstract = "The rising incidence of antibiotic resistant microorganisms urges novel antimicrobials development with polyphenols as appealing potential therapeutics. We aimed to reveal the most promising polyphenols among hesperetin, hesperidin, naringenin, naringin, taxifolin, rutin, isoquercitrin, morin, chlorogenic acid, ferulic acid, p-coumaric acid, and gallic acid based on antimicrobial capacity, antibiofilm potential, and lack of cytotoxicity towards HaCaT, and to further test its antivirulence mechanisms. Although the majority of studied polyphenols were able to inhibit bacterial growth and biofilm formation, the most promising activities were observed for rutin. Further investigation proved rutin's ability to prevent/eradicate Pseudomonas aeruginosa and MRSA urinary catheter biofilms. Besides reduction of biofilm biomass, rutin antibiofilm mechanisms included reduction of cell viability, exopolysaccharide, and extracellular DNA levels. Moderate reduction of bacterial adhesion to human keratinocytes upon treatment was observed. Rutin antivirulence mechanisms included an impact on P. aeruginosa protease, pyocyanin, rhamnolipid, and elastase production and the downregulation of the lasI, lasR, rhlI, rhlR, pqsA and mvfR genes. Rutin also interfered with membrane permeability. Polyphenols could repress antibiotic resistant bacteria. Rutin has shown wide antimicrobial and antibiofilm capacity employing a range of mechanisms that might be used for the development of novel antimicrobials.",
publisher = "Basel: MDPI",
journal = "Pharmaceuticals",
title = "Polyphenols as inhibitors of antibiotic resistant bacteria - Mechanisms underlying rutin interference with bacterial virulence",
number = "3",
volume = "15",
doi = "10.3390/ph15030385",
pages = "385"
}
Ivanov, M., Novović, K., Malešević, M., Dinić, M., Stojković, D., Jovčić, B.,& Soković, M.. (2022). Polyphenols as inhibitors of antibiotic resistant bacteria - Mechanisms underlying rutin interference with bacterial virulence. in Pharmaceuticals
Basel: MDPI., 15(3), 385.
https://doi.org/10.3390/ph15030385
Ivanov M, Novović K, Malešević M, Dinić M, Stojković D, Jovčić B, Soković M. Polyphenols as inhibitors of antibiotic resistant bacteria - Mechanisms underlying rutin interference with bacterial virulence. in Pharmaceuticals. 2022;15(3):385.
doi:10.3390/ph15030385 .
Ivanov, Marija, Novović, Katarina, Malešević, Milka, Dinić, Miroslav, Stojković, Dejan, Jovčić, Branko, Soković, Marina, "Polyphenols as inhibitors of antibiotic resistant bacteria - Mechanisms underlying rutin interference with bacterial virulence" in Pharmaceuticals, 15, no. 3 (2022):385,
https://doi.org/10.3390/ph15030385 . .
2
30

Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.

Stanisavljević, Suzana; Dinić, Miroslav; Jevtić, Bojan; Nikolovski, Neda; Momčilović, Miljana; Đokić, Jelena; Golić, Nataša; Mostarica Stojković, Marija; Miljković, Đorđe

(2018)

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Dinić, Miroslav
AU  - Jevtić, Bojan
AU  - Nikolovski, Neda
AU  - Momčilović, Miljana
AU  - Đokić, Jelena
AU  - Golić, Nataša
AU  - Mostarica Stojković, Marija
AU  - Miljković, Đorđe
PY  - 2018
UR  - http://journal.frontiersin.org/article/10.3389/fimmu.2018.00942/full
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5942155
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3056
AB  - Albino Oxford (AO) rats are extremely resistant to induction of experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of multiple sclerosis, a chronic inflammatory disease of the central nervous system (CNS), with established autoimmune pathogenesis. The autoimmune response against the antigens of the CNS is initiated in the peripheral lymphoid tissues after immunization of AO rats with CNS antigens. Subsequently, limited infiltration of the CNS occurs, yet without clinical sequels. It has recently become increasingly appreciated that gut-associated lymphoid tissues (GALT) and gut microbiota play an important role in regulation and propagation of encephalitogenic immune response. Therefore, modulation of AO gut microbiota by antibiotics was performed in this study. The treatment altered composition of gut microbiota in AO rats and led to a reduction in the proportion of regulatory T cells in Peyer's patches, mesenteric lymph nodes, and in lymph nodes draining the site of immunization. Upregulation of interferon-γ and interleukin (IL)-17 production was observed in the draining lymph nodes. The treatment led to clinically manifested EAE in AO rats with more numerous infiltrates and higher production of IL-17 observed in the CNS. Importantly, transfer of AO gut microbiota into EAE-prone Dark Agouti rats ameliorated the disease. These results clearly imply that gut microbiota is an important factor in AO rat resistance to EAE and that gut microbiota transfer is an efficacious way to treat CNS autoimmunity. These findings also support the idea that gut microbiota modulation has a potential as a future treatment of multiple sclerosis.
T2  - Frontiers in Immunology
T1  - Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.
VL  - 9
DO  - 10.3389/fimmu.2018.00942
SP  - 942
ER  - 
@article{
author = "Stanisavljević, Suzana and Dinić, Miroslav and Jevtić, Bojan and Nikolovski, Neda and Momčilović, Miljana and Đokić, Jelena and Golić, Nataša and Mostarica Stojković, Marija and Miljković, Đorđe",
year = "2018",
abstract = "Albino Oxford (AO) rats are extremely resistant to induction of experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of multiple sclerosis, a chronic inflammatory disease of the central nervous system (CNS), with established autoimmune pathogenesis. The autoimmune response against the antigens of the CNS is initiated in the peripheral lymphoid tissues after immunization of AO rats with CNS antigens. Subsequently, limited infiltration of the CNS occurs, yet without clinical sequels. It has recently become increasingly appreciated that gut-associated lymphoid tissues (GALT) and gut microbiota play an important role in regulation and propagation of encephalitogenic immune response. Therefore, modulation of AO gut microbiota by antibiotics was performed in this study. The treatment altered composition of gut microbiota in AO rats and led to a reduction in the proportion of regulatory T cells in Peyer's patches, mesenteric lymph nodes, and in lymph nodes draining the site of immunization. Upregulation of interferon-γ and interleukin (IL)-17 production was observed in the draining lymph nodes. The treatment led to clinically manifested EAE in AO rats with more numerous infiltrates and higher production of IL-17 observed in the CNS. Importantly, transfer of AO gut microbiota into EAE-prone Dark Agouti rats ameliorated the disease. These results clearly imply that gut microbiota is an important factor in AO rat resistance to EAE and that gut microbiota transfer is an efficacious way to treat CNS autoimmunity. These findings also support the idea that gut microbiota modulation has a potential as a future treatment of multiple sclerosis.",
journal = "Frontiers in Immunology",
title = "Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.",
volume = "9",
doi = "10.3389/fimmu.2018.00942",
pages = "942"
}
Stanisavljević, S., Dinić, M., Jevtić, B., Nikolovski, N., Momčilović, M., Đokić, J., Golić, N., Mostarica Stojković, M.,& Miljković, Đ.. (2018). Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.. in Frontiers in Immunology, 9, 942.
https://doi.org/10.3389/fimmu.2018.00942
Stanisavljević S, Dinić M, Jevtić B, Nikolovski N, Momčilović M, Đokić J, Golić N, Mostarica Stojković M, Miljković Đ. Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis.. in Frontiers in Immunology. 2018;9:942.
doi:10.3389/fimmu.2018.00942 .
Stanisavljević, Suzana, Dinić, Miroslav, Jevtić, Bojan, Nikolovski, Neda, Momčilović, Miljana, Đokić, Jelena, Golić, Nataša, Mostarica Stojković, Marija, Miljković, Đorđe, "Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis." in Frontiers in Immunology, 9 (2018):942,
https://doi.org/10.3389/fimmu.2018.00942 . .
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