| First Author | Upadhyay V | Year | 2012 |
| Journal | Nat Immunol | Volume | 13 |
| Issue | 10 | Pages | 947-53 |
| PubMed ID | 22922363 | Mgi Jnum | J:187700 |
| Mgi Id | MGI:5437801 | Doi | 10.1038/ni.2403 |
| Citation | Upadhyay V, et al. (2012) Lymphotoxin regulates commensal responses to enable diet-induced obesity. Nat Immunol 13(10):947-53 |
| abstractText | Microbiota are essential for weight gain in mouse models of diet-induced obesity (DIO), but the pathways that cause the microbiota to induce weight gain are unknown. We report that mice deficient in lymphotoxin, a key molecule in gut immunity, were resistant to DIO. Ltbr(-/-) mice had different microbial community composition compared to their heterozygous littermates, including an overgrowth of segmented filamentous bacteria (SFB). Furthermore, cecal transplantation conferred leanness to germ-free recipients. Housing Ltbr(-/-) mice with their obese siblings rescued weight gain in Ltbr(-/-) mice, demonstrating the communicability of the obese phenotype. Ltbr(-/-) mice lacked interleukin 23 (IL-23) and IL-22, which can regulate SFB. Mice deficient in these pathways also resisted DIO, demonstrating that intact mucosal immunity guides diet-induced changes to the microbiota to enable obesity. |
