Perturbation of the gut microbiome by Prevotella spp. enhances host susceptibility to mucosal inflammation.
Perturbation of the gut microbiome by Prevotella spp. enhances host susceptibility to mucosal inflammation.
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DOI：
10.1038/s41385-020-0296-4
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发表时间：
2021-01
影响因子：
8
通讯作者：
Strowig T
中科院分区：
文献类型：
--
作者：
Iljazovic A;Roy U;Gálvez EJC;Lesker TR;Zhao B;Gronow A;Amend L;Will SE;Hofmann JD;Pils MC;Schmidt-Hohagen K;Neumann-Schaal M;Strowig T
肠道微生物群中的多种微生物特征与肠道和全身性炎症性疾病相关，但这些候选微生物是否主动调节宿主表型或在改变的微生物生态系统中被动扩增通常尚不清楚。在这里，我们证明，殖民化的小鼠与普雷沃氏菌属的成员，这是以前与结肠炎的小鼠，加剧肠道炎症。我们的分析表明，普雷沃氏菌改变了生态系统的组成和功能，导致短链脂肪酸，特别是乙酸酯的减少，因此在稳态期间肠道IL-18水平降低。补充IL-18到Prevotella定殖的小鼠足以减少肠道炎症。因此，我们得出结论，肠道普雷沃氏菌定殖导致微生物群的代谢变化，这减少了IL-18的产生，从而加剧了肠道炎症和潜在的全身性自身免疫。
Diverse microbial signatures within the intestinal microbiota have been associated with intestinal and systemic inflammatory diseases, but whether these candidate microbes actively modulate host phenotypes or passively expand within the altered microbial ecosystem is frequently not known. Here we demonstrate that colonization of mice with a member of the genus Prevotella, which has been previously associated to colitis in mice, exacerbates intestinal inflammation. Our analysis revealed that Prevotella intestinalis alters composition and function of the ecosystem resulting in a reduction of short-chain fatty acids, specifically acetate, and consequently a decrease in intestinal IL-18 levels during steady state. Supplementation of IL-18 to Prevotella-colonized mice was sufficient to reduce intestinal inflammation. Hence, we conclude that intestinal Prevotella colonization results in metabolic changes in the microbiota, which reduce IL-18 production and consequently exacerbate intestinal inflammation, and potential systemic autoimmunity.
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常见的小鼠原生动物Tritrichomonas muris改变了粘膜T细胞稳态和结肠炎的敏感性。
DOI：
10.1084/jem.20161776
发表时间：
2016-12-12
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Escalante NK;Lemire P;Cruz Tleugabulova M;Prescott D;Mortha A;Streutker CJ;Girardin SE;Philpott DJ;Mallevaey T
通讯作者：
Mallevaey T
影响因子：
64.8
作者：
Arumugam, Manimozhiyan;Raes, Jeroen;Pelletier, Eric;Le Paslier, Denis;Yamada, Takuji;Mende, Daniel R.;Fernandes, Gabriel R.;Tap, Julien;Bruls, Thomas;Batto, Jean-Michel;Bertalan, Marcelo;Borruel, Natalia;Casellas, Francesc;Fernandez, Leyden;Gautier, Laurent;Hansen, Torben;Hattori, Masahira;Hayashi, Tetsuya;Kleerebezem, Michiel;Kurokawa, Ken;Leclerc, Marion;Levenez, Florence;Manichanh, Chaysavanh;Nielsen, H. Bjorn;Nielsen, Trine;Pons, Nicolas;Poulain, Julie;Qin, Junjie;Sicheritz-Ponten, Thomas;Tims, Sebastian;Torrents, David;Ugarte, Edgardo;Zoetendal, Erwin G.;Wang, Jun;Guarner, Francisco;Pedersen, Oluf;de Vos, Willem M.;Brunak, Soren;Dore, Joel;Weissenbach, Jean;Ehrlich, S. Dusko;Bork, Peer
通讯作者：
Bork, Peer
影响因子：
29
作者：
De Vadder, Filipe;Kovatcheva-Datchary, Petia;Mithieux, Gilles
通讯作者：
Mithieux, Gilles
影响因子：
64.5
作者：
Chung H;Pamp SJ;Hill JA;Surana NK;Edelman SM;Troy EB;Reading NC;Villablanca EJ;Wang S;Mora JR;Umesaki Y;Mathis D;Benoist C;Relman DA;Kasper DL
通讯作者：
Kasper DL
影响因子：
3.1
作者：
Barthel, M;Hapfelmeier, S;Hardt, WD
通讯作者：
Hardt, WD