The common mouse protozoa Tritrichomonas muris alters mucosal T cell homeostasis and colitis susceptibility.
The common mouse protozoa Tritrichomonas muris alters mucosal T cell homeostasis and colitis susceptibility.
复制标题
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
复制
发表时间:
2016-12-12
期刊:
影响因子:
--
通讯作者:
Mallevaey T
中科院分区:
文献类型:
--
作者:
Escalante NK;Lemire P;Cruz Tleugabulova M;Prescott D;Mortha A;Streutker CJ;Girardin SE;Philpott DJ;Mallevaey T
Escalante et al. show that a highly prevalent mouse intestinal protozoa, Tritrichomonas muris, was found to be a confounding factor in murine colitis. Mice infected with this parasite had elevated baseline levels of Th1 cytokines and developed exacerbated Th1-mediated disease. The mammalian gastrointestinal tract hosts a diverse community of microbes including bacteria, fungi, protozoa, helminths, and viruses. Through coevolution, mammals and these microbes have developed a symbiosis that is sustained through the host’s continuous sensing of microbial factors and the generation of a tolerant or pro-inflammatory response. While analyzing T cell–driven colitis in nonlittermate mouse strains, we serendipitously identified that a nongenetic transmissible factor dramatically increased disease susceptibility. We identified the protozoan Tritrichomonas muris as the disease-exacerbating element. Furthermore, experimental colonization with T. muris induced an elevated Th1 response in the cecum of naive wild-type mice and accelerated colitis in Rag1−/− mice after T cell transfer. Overall, we describe a novel cross-kingdom interaction within the murine gut that alters immune cell homeostasis and disease susceptibility. This example of unpredicted microbial priming of the immune response highlights the importance of studying trans-kingdom interactions and serves as a stark reminder of the importance of using littermate controls in all mouse research.
登录
查看更多内容
DOI:
10.1126/science.aad5872
发表时间:
2016-01-15
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Pfeiffer JK;Virgin HW
通讯作者:
Virgin HW
影响因子:
56.9
作者:
Karst, SM;Wobus, CE;Virgin, HW
通讯作者:
Virgin, HW
影响因子:
2.4
作者:
ROACH, PD;WALLIS, PM;OLSON, ME
通讯作者:
OLSON, ME
DOI:
10.1126/science.aaf1648
发表时间:
2016-03-18
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Howitt MR;Lavoie S;Michaud M;Blum AM;Tran SV;Weinstock JV;Gallini CA;Redding K;Margolskee RF;Osborne LC;Artis D;Garrett WS
通讯作者:
Garrett WS
影响因子:
64.5
作者:
Chudnovskiy, Aleksey;Mortha, Arthur;Kana, Veronika;Kennard, Andrea;Ramirez, Juan David;Rahman, Adeeb;Remark, Romain;Mogno, Ilaria;Ng, Ruby;Gnjatic, Sasha;Amir, El-ad David;Solovyov, Alexander;Greenbaum, Benjamin;Clemente, Jose;Faith, Jeremiah;Belkaid, Yasmine;Grigg, Michael E.;Merad, Miriam
通讯作者:
Merad, Miriam