Science 26 Jul 2019:
Vol. 365, Issue 6451, eaat9351
DOI: 10.1126/science.aat9351
Author:
Charisse Petersen1, Rickesha Bell1, Kendra A. Klag1, Soh-Hyun Lee1, Raymond Soto1, Arevik Ghazaryan1, Kaitlin Buhrke1, H. Atakan Ekiz1, Kyla S. Ost1, Sihem Boudina2, Ryan M. O’Connell1, James E. Cox3, Claudio J. Villanueva3, W. Zac Stephens1,*, June L. Round1,*
Abstract:
The microbiota influences obesity, yet organisms that protect from disease remain unknown. During studies interrogating host-microbiota interactions, we observed the development of age-associated metabolic syndrome (MetS). Expansion of Desulfovibrio and loss of Clostridia were key features associated with obesity in this model and are present in humans with MetS. T cell–dependent events were required to prevent disease, and replacement of Clostridia rescued obesity. Inappropriate immunoglobulin A targeting of Clostridia and increased Desulfovibrio antagonized the colonization of beneficial Clostridia. Transcriptional and metabolic analysis revealed enhanced lipid absorption in the obese host. Colonization of germ-free mice with Clostridia, but not Desulfovibrio, down-regulated genes that control lipid absorption and reduced adiposity. Thus, immune control of the microbiota maintains beneficial microbial populations that constrain lipid metabolism to prevent MetS.
指導教授：徐堯煇、王敏盈 教授
報告序號：20191121-2
組員：生技碩二 李翊誠
生技碩一 林佩誼
