title: Vitamin A metabolism and mucosal immune function are distinct between BALB/c and C57BL/6 mice.
abstract: The vitamin A metabolite retinoic acid (RA) has been reported to suppress Th1 responses and enhance Th2 responses. Here, we investigated whether differences in vitamin A metabolism could underlie the differences between C57BL/6 and BALB/c mice, which are reportedly seen as Th1 and Th2 responders, respectively. BALB/c mice were shown to have higher intestinal epithelial expression of RALDH1 (where RALDH is retinaldehyde dehydrogenase), and, consequently, higher RALDH activity in MLN-DCs, leading to an increased ability to induce IgA class switching in B cells. Furthermore, within BALB/c mice, induction of IgA secretion as well as increased accumulation of regulatory T cells (Treg) in the intestinal lamina propria was observed. Additionally, as BALB/c mice are more resistant to dextran sulphate sodium (DSS) induced colitis, mice that lacked vitamin A in their diet had a more severe form of DSS-induced colitis compared to control mice. Therefore, the level of RA production and consequently the degree of RA-mediated signaling is crucial for the efficiency of the mucosal immune system.
authors.affiliation: Department of Molecular Cell Biology and Immunology, VU medical center, Amsterdam, The Netherlands.
authors.forename: Gera
authors.initials: G
authors.lastname: Goverse
authors.forename: Brenda J
authors.initials: BJ
authors.lastname: Olivier
authors.forename: Rosalie
authors.initials: R
authors.lastname: Molenaar
authors.forename: Marlene
authors.initials: M
authors.lastname: Knippenberg
authors.forename: Mascha
authors.initials: M
authors.lastname: Greuter
authors.forename: Tanja
authors.initials: T
authors.lastname: Konijn
authors.forename: Emma C L
authors.initials: EC
authors.lastname: Cook
authors.forename: Marieke R
authors.initials: MR
authors.lastname: Beijer
authors.forename: Dawn M
authors.initials: DM
authors.lastname: Fedor
authors.forename: Joke M M
authors.initials: JM
authors.lastname: den Haan
authors.forename: Joseph L
authors.initials: JL
authors.lastname: Napoli
authors.forename: Gerd
authors.initials: G
authors.lastname: Bouma
authors.forename: Reina E
authors.initials: RE
authors.lastname: Mebius
mesh_terms: D000080924:Aldehyde Dehydrogenase 1 Family; D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016264:Dextran Sulfate; D015870:Gene Expression; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D017578:Immunoglobulin Class Switching; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000276:immunology* / Q000473:pathology; D007527:Isoenzymes / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009092:Mucous Membrane / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D050697:Retinal Dehydrogenase / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction; D013045:Species Specificity; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D014801:Vitamin A / Q000008:administration & dosage / Q000378:metabolism*
chemical_list: D007070:Immunoglobulin A; D007527:Isoenzymes; D014801:Vitamin A; D016264:Dextran Sulfate; D000080924:Aldehyde Dehydrogenase 1 Family; C515028:ALDH1A1 protein, mouse; D050697:Retinal Dehydrogenase
keywords: BALB/c; C57BL/6; FoxP3; IgA; Intestine; Retinaldehyde dehydrogenase; Vitamin A