| Budget Amount *help |
¥16,280,000 (Direct Cost: ¥14,900,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2007: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2006: ¥10,300,000 (Direct Cost: ¥10,300,000)
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| Research Abstract |
Intestinal commensal bacteria play important roles in the regulation of intestinal immune responses such as anti-allergic reaction and anti-infection. It has been shown that intestinal commensal bacteria greatly affect the development of gut-associated lymphoid tissues and mucosal immune responses, such as IgA production, in the gut. Given the large numbers of intestinal microbiota, particularly in the large intestine, it is believed that immunocytes in the large intestine are modulated by microbacteria. While IgA production by immunocytes in the small intestine has been previously studied, IgA production in the large intestine is, however, poorly understood. In this study, we show that IgA production by lymphocytes is induced by microbacteria present in the large intestine.
Lamina propria lymphocytes from the large intestine (L-LP) were isolated from germ-free (GF) and conventional (CV) mice. Flow cytometric analysis of L-LP lymphocytes was used to assess the frequency of IgM+B220+ cel
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ls, IgA+B220+ cells, and IgA+Syndecan-l+B220- cells. In addition, to determine whether stimulation by commensal bacteria influences differentiation of IgM+ cells into IgA-plasma cells, IgM+ cells separated from L-LP lymphocytes of GF mice were co-cultured with Bacteroides acidofaciens isolated from intestinal commensal bacteria of CV mice.
The frequency of IgA+Syndecan-1+B220- cells and IgA+B220+ cells in L-LP of GF were all lower than that of CV mice, but there was no difference in the frequency of IgM+13220+ cells in L-LP between GF and CV mice. IgA production by IgM+ cells stimulated by B. acidofaciens was higher than in those without bacterial stimulation.
These results indicate that direct stimulation by B. acidofaciens induces differentiation of IgM+ cells into IgA-producing plasma cells from the large intestine. These also suggest that IgA production in the large intestine might be induced by intestinal commensal bacteria, thus intestinal microbacteria promote the class switching from IgM to IgA in the large intestine. Less
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