Abstract
M cells in follicle-associated epithelium (FAE) are specialized antigen-sampling cells that take up intestinal luminal antigens. Transcription factor Spi-B regulates M-cell maturation, but the molecules that promote transcytosis within M cells are not fully identified. Here we show that mouse allograft inflammatory factor 1 (Aif1) is expressed by M cells and contributes to M-cell transcytosis. FAE in Aif1 -/- mice has suppressed uptake of particles and commensal bacteria, compared with wild-type mice. Translocation of Yersinia enterocolitica, but not of Salmonella enterica serovar Typhimurium, leading to the generation of antigen-specific IgA antibodies, is also diminished in Aif1-deficient mice. Although β1 integrin, which acts as a receptor for Y. enterocolitica via invasin protein, is expressed on the apical surface membranes of M cells, its active form is rarely found in Aif1 -/- mice. These findings show that Aif1 is important for bacterial and particle transcytosis in M cells.
| Original language | English |
|---|---|
| Article number | 14509 |
| Journal | Nature communications |
| Volume | 8 |
| DOIs | |
| Publication status | Published - Feb 22 2017 |
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All Science Journal Classification (ASJC) codes
- Chemistry(all)
- Biochemistry, Genetics and Molecular Biology(all)
- Physics and Astronomy(all)
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Allograft inflammatory factor 1 is a regulator of transcytosis in M cells. / Kishikawa, Sari; Sato, Shintaro S.S.; Kaneto, Satoshi; Uchino, Shigeo; Kohsaka, Shinichi; Nakamura, Seiji; Kiyono, Hiroshi.
In: Nature communications, Vol. 8, 14509, 22.02.2017.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Allograft inflammatory factor 1 is a regulator of transcytosis in M cells
AU - Kishikawa, Sari
AU - Sato, Shintaro S.S.
AU - Kaneto, Satoshi
AU - Uchino, Shigeo
AU - Kohsaka, Shinichi
AU - Nakamura, Seiji
AU - Kiyono, Hiroshi
PY - 2017/2/22
Y1 - 2017/2/22
N2 - M cells in follicle-associated epithelium (FAE) are specialized antigen-sampling cells that take up intestinal luminal antigens. Transcription factor Spi-B regulates M-cell maturation, but the molecules that promote transcytosis within M cells are not fully identified. Here we show that mouse allograft inflammatory factor 1 (Aif1) is expressed by M cells and contributes to M-cell transcytosis. FAE in Aif1 -/- mice has suppressed uptake of particles and commensal bacteria, compared with wild-type mice. Translocation of Yersinia enterocolitica, but not of Salmonella enterica serovar Typhimurium, leading to the generation of antigen-specific IgA antibodies, is also diminished in Aif1-deficient mice. Although β1 integrin, which acts as a receptor for Y. enterocolitica via invasin protein, is expressed on the apical surface membranes of M cells, its active form is rarely found in Aif1 -/- mice. These findings show that Aif1 is important for bacterial and particle transcytosis in M cells.
AB - M cells in follicle-associated epithelium (FAE) are specialized antigen-sampling cells that take up intestinal luminal antigens. Transcription factor Spi-B regulates M-cell maturation, but the molecules that promote transcytosis within M cells are not fully identified. Here we show that mouse allograft inflammatory factor 1 (Aif1) is expressed by M cells and contributes to M-cell transcytosis. FAE in Aif1 -/- mice has suppressed uptake of particles and commensal bacteria, compared with wild-type mice. Translocation of Yersinia enterocolitica, but not of Salmonella enterica serovar Typhimurium, leading to the generation of antigen-specific IgA antibodies, is also diminished in Aif1-deficient mice. Although β1 integrin, which acts as a receptor for Y. enterocolitica via invasin protein, is expressed on the apical surface membranes of M cells, its active form is rarely found in Aif1 -/- mice. These findings show that Aif1 is important for bacterial and particle transcytosis in M cells.
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UR - http://www.scopus.com/inward/citedby.url?scp=85013671189&partnerID=8YFLogxK
U2 - 10.1038/ncomms14509
DO - 10.1038/ncomms14509
M3 - Article
C2 - 28224999
AN - SCOPUS:85013671189
VL - 8
JO - Nature Communications
JF - Nature Communications
SN - 2041-1723
M1 - 14509
ER -