- Petersen, Charisse;
- Bell, Rickesha;
- Klag, Kendra A;
- Lee, Soh-Hyun;
- Soto, Raymond;
- Ghazaryan, Arevik;
- Buhrke, Kaitlin;
- Ekiz, H Atakan;
- Ost, Kyla S;
- Boudina, Sihem;
- O'Connell, Ryan M;
- Cox, James E;
- Villanueva, Claudio J;
- Stephens, W Zac;
- Round, June L
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.