title: IgA production in the large intestine is modulated by a different mechanism than in the small intestine: Bacteroides acidifaciens promotes IgA production in the large intestine by inducing germinal center formation and increasing the number of IgA+ B cells.
abstract: It has been demonstrated that intestinal commensal bacteria induce immunoglobulin (Ig) A production by promoting the development of gut-associated lymphoid tissues in the small intestine. However, the precise mechanism whereby these bacteria modulate IgA production in the large intestine, which harbors the majority of intestinal commensals, is poorly understood. In addition, it is not known which commensal bacteria induce IgA production in the small intestine and which induce production in the large intestine. To address these issues, we generated gnotobiotic mice mono-associated with different murine commensal bacteria by inoculating germ-free (GF) mice with Lactobacillus johnsonii or Bacteroides acidifaciens. In GF mice, IgA production was barely detectable in the small intestine and was not detected in the large intestine. Interestingly, total IgA secretion in the large intestinal mucosa of B. acidifaciens mono-associated (BA) mice was significantly greater than that of GF and L. johnsonii mono-associated (LJ) mice. However, there was no difference in total IgA production in the small intestine of GF, LJ and BA mice. In addition, in the large intestine of BA mice, the expression of IgA(+) cells and germinal center formation were more remarkable than in GF and LJ mice. Furthermore, B. acidifaciens-specific IgA was detected in the large intestine of BA mice. These results suggest that the production of IgA in the large intestine may be modulated by a different mechanism than that in the small intestine, and that B. acidifaciens is one of the predominant bacteria responsible for promoting IgA production in the large intestine.
authors.affiliation: Department of Food Bioscience and Biotechnology, College of Bioresource Sciences, Nihon University, Kanagawa 252-0880, Japan.
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Yanagibashi
authors.forename: Akira
authors.initials: A
authors.lastname: Hosono
authors.forename: Akihito
authors.initials: A
authors.lastname: Oyama
authors.forename: Masato
authors.initials: M
authors.lastname: Tsuda
authors.forename: Ami
authors.initials: A
authors.lastname: Suzuki
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hachimura
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Yoshika
authors.initials: Y
authors.lastname: Momose
authors.forename: Kikuji
authors.initials: K
authors.lastname: Itoh
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Hirayama
authors.forename: Kyoko
authors.initials: K
authors.lastname: Takahashi
authors.forename: Shuichi
authors.initials: S
authors.lastname: Kaminogawa
mesh_terms: D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D001439:Bacteroides / Q000276:immunology*; D001442:Bacteroides Infections / Q000276:immunology* / Q000382:microbiology; D018858:Germinal Center / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000096:biosynthesis / Q000276:immunology*; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D007420:Intestine, Large / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D007421:Intestine, Small / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D007778:Lactobacillus / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009928:Organ Specificity / Q000276:immunology
chemical_list: D007070:Immunoglobulin A