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Nat Immunol. 2012 Oct;13(10):947-53. doi: 10.1038/ni.2403. Epub 2012 Aug 26.

Lymphotoxin regulates commensal responses to enable diet-induced obesity.

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1
Department of Pathology and Committee on Immunology, The University of Chicago, Chicago, Illinois, USA.

Abstract

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.

PMID:
22922363
PMCID:
PMC3718316
DOI:
10.1038/ni.2403
[Indexed for MEDLINE]
Free PMC Article
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