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Bacterial Flora Play Important Roles in Acute Dextran Sulphate Sodium-Induced Colitis But Are Not Involved in Gal-3 Dependent Modulation of Colon Inflammation Cover

Bacterial Flora Play Important Roles in Acute Dextran Sulphate Sodium-Induced Colitis But Are Not Involved in Gal-3 Dependent Modulation of Colon Inflammation

Open Access
|Oct 2017

Abstract

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 infl ammasome 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 microfl ora. 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.

DOI: https://doi.org/10.1515/sjecr-2017-0022 | Journal eISSN: 2956-2090 | Journal ISSN: 2956-0454
Language: English
Page range: 213 - 220
Submitted on: Dec 19, 2016
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Accepted on: Feb 1, 2016
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Published on: Oct 19, 2017
In partnership with: Paradigm Publishing Services
Publication frequency: 4 issues per year

© 2017 Bojana Simovic Markovic, Neda Milosavljevic, Aleksandar Arsenijevic, Marina Gazdic, Miodrag L. Lukic, Vladislav Volarevic, published by University of Kragujevac, Faculty of Medical Sciences
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.