Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/8749
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dc.rights.licenseBY-NC-ND-
dc.contributor.authorMarkovic B.-
dc.contributor.authorMilosavljevic N.-
dc.contributor.authorArsenijevic A.-
dc.contributor.authorGazdic, Marina-
dc.contributor.authorLukic, Miodrag-
dc.contributor.authorVolarevic, Vladislav-
dc.date.accessioned2020-09-19T16:35:31Z-
dc.date.available2020-09-19T16:35:31Z-
dc.date.issued2017-
dc.identifier.issn1820-8665-
dc.identifier.urihttps://scidar.kg.ac.rs/handle/123456789/8749-
dc.description.abstract© 2017, University of Kragujevac, Faculty of Science. All rights reserved. An altered immune response to normal gut microflora is important for the pathogenesis of ulcerative colitis (UC). Galectin- 3 (Gal-3) is an endogenous lectin that plays an important pro-inflammatory role in the induction phase of acute colitis by promoting activation of the NLRP3 inflammasome and production of IL-1β in macrophages. By using dextran sulphate sodium (DSS) induced colitis, a well-established animal model of UC, we determined whether Gal-3 affects the function of colon infiltrating macrophages by interfering with intestinal microflora. Our results showed that genetic deletion of Gal-3 significantly attenuates DSS-induced colitis by down-regulating infiltration of phagocytic cells (neutrophils, macrophages and dendritic cells) in colon tissue of DSS-treated mice, and this correlated with differences in bacterial flora of the gut. Antibiotic treatment attenuates DSS-induced colitis in WT and Gal-3-/- mice without affecting differences between the groups. In conclusion, Gram negative bacterial flora play an important role in DSS-induced acute colitis of mice but are not involved in Gal-3 dependent modulation of colon inflammation.-
dc.rightsopenAccess-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.sourceSerbian Journal of Experimental and Clinical Research-
dc.titleBacterial flora play important roles in acute dextran sulphate sodium-induced colitis but are not involved in Gal-3 dependent modulation of colon inflammation-
dc.typearticle-
dc.identifier.doi10.1515/SJECR-2017-0022-
dc.identifier.scopus2-s2.0-85030680699-
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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