Immunomodulation by Bifidobacterium infantis 35624 in the murine lamina propria requires retinoic acid-dependent and independent mechanisms.

Abstract

Appropriate dendritic cell processing of the microbiota promotes intestinal homeostasis and protects against aberrant inflammatory responses. Mucosal CD103(+) dendritic cells are able to produce retinoic acid from retinal, however their role in vivo and how they are influenced by specific microbial species has been poorly described. Bifidobacterium infantis 35624 (B. infantis) feeding to mice resulted in increased numbers of CD103(+)retinaldehyde dehydrogenase (RALDH)(+) dendritic cells within the lamina propria (LP). Foxp3(+) lymphocytes were also increased in the LP, while TH1 and TH17 subsets were decreased. 3,7-dimethyl-2,6-octadienal (citral) treatment of mice blocked the increase in CD103(+)RALDH(+) dendritic cells and the decrease in TH1 and TH17 lymphocytes, but not the increase in Foxp3(+) lymphocytes. B. infantis reduced the severity of DSS-induced colitis, associated with decreased TH1 and TH17 cells within the LP. Citral treatment confirmed that these effects were RALDH mediated. RALDH(+) dendritic cells decreased within the LP of control inflamed animals, while RALDH(+) dendritic cells numbers were maintained in the LP of B. infantis-fed mice. Thus, CD103(+)RALDH(+) LP dendritic cells are important cellular targets for microbiota-associated effects on mucosal immunoregulation.