Diet Rich in Animal Protein Promotes Pro-inflammatory Macrophage Response and Exacerbates Colitis in Mice

0579096 - ÚMG 2024 RIV CH eng J - Článek v odborném periodiku
Kostovčíková, Klára - Coufal, Š. - Galanová, N. - Fajstová, A. - Hudcovic, T. - Kostovčík, M. - Procházková, P. - Zákostelská, Z. - Čermáková, M. - Šedivá, B. - Kuzma, M. - Tlaskalová-Hogenová, H. - Kverka, M.
Diet Rich in Animal Protein Promotes Pro-inflammatory Macrophage Response and Exacerbates Colitis in Mice.
Frontiers in Immunology. Roč. 10, Apr (2019), č. článku 919. ISSN 1664-3224. E-ISSN 1664-3224
Institucionální podpora: RVO:68378050
Klíčová slova: gut microbiota * dextran sulfate * intestinal inflammation * bowel-disease * luminal environment * ulcerative-colitis * fatty-acids * supplementation * communities * metabolites * dietary protein * microbiota * colitis * germ-free * macrophage
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 5.085, rok: 2019
Způsob publikování: Open access
https://www.frontiersin.org/articles/10.3389/fimmu.2019.00919/full

Diet is a major factor determining gut microbiota composition and perturbances in this complex ecosystem are associated with the inflammatory bowel disease (IBD). Here, we used gnotobiotic approach to analyze, how interaction between diet rich in proteins and gut microbiota influences the sensitivity to intestinal inflammation in murine model of ulcerative colitis. We found that diet rich in animal protein (aHPD) exacerbates acute dextran sulfate sodium (DSS)-induced colitis while diet rich in plant protein (pHPD) does not. The deleterious effect of aHPD was also apparent in chronic DSS colitis and was associated with distinct changes in gut bacteria and fungi. Therefore, we induced acute DSS-colitis in germ-free mice and transferred gut microbiota from aCD or aHPD fed mice to find that this effect requires presence of microbes and aHPD at the same time. The aHPD did not change the number of regulatory T cells or Th17 cells and still worsened the colitis in immuno-deficient RAG2 knock-out mice suggesting that this effect was not dependent on adaptive immunity. The pro-inflammatory effect of aHPD was, however, abrogated when splenic macrophages were depleted with clodronate liposomes. This treatment prevented aHPD induced increase in colonic Ly-6C(high) pro-inflammatory monocytes, but the ratio of resident Ly-6C(-/low) macrophages was not changed. These data show that the interactions between dietary protein of animal origin and gut microbiota increase sensitivity to intestinal inflammation by promoting pro-inflammatory response of monocytes.
Trvalý link: https://hdl.handle.net/11104/0347961