Disruption of the intestinal barrier exacerbates experimental autoimmune pancreatitis by promoting the translocation of<i>Staphylococcus sciuri</i>into the pancreas
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- Tomoe Yoshikawa
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Kosuke Minaga
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Akane Hara
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Ikue Sekai
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Masayuki Kurimoto
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Yasuhiro Masuta
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Yasuo Otsuka
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Ryutaro Takada
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Ken Kamata
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Ah-Mee Park
- Department of Microbiology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Shiki Takamura
- Department of Immunology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Masatoshi Kudo
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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- Tomohiro Watanabe
- Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511 , Japan
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<jats:title>Abstract</jats:title><jats:p>Autoimmune pancreatitis (AIP) and IgG4-related disease (IgG4-RD) are new disease entities characterized by enhanced IgG4 antibody responses and involvement of multiple organs, including the pancreas and salivary glands. Although the immunopathogenesis of AIP and IgG4-RD is poorly understood, we previously reported that intestinal dysbiosis mediates experimental AIP through the activation of IFN-α- and IL-33-producing plasmacytoid dendritic cells (pDCs). Because intestinal dysbiosis is linked to intestinal barrier dysfunction, we explored whether the latter affects the development of AIP and autoimmune sialadenitis in MRL/MpJ mice treated with repeated injections of polyinosinic–polycytidylic acid [poly (I:C)]. Epithelial barrier disruption was induced by the administration of dextran sodium sulfate (DSS) in the drinking water. Mice co-treated with poly (I:C) and DSS, but not those treated with either agent alone, developed severe AIP, but not autoimmune sialadenitis, which was accompanied by the increased accumulation of IFN-α- and IL-33-producing pDCs. Sequencing of 16S ribosomal RNA revealed that Staphylococcus sciuri translocation from the gut to the pancreas was preferentially observed in mice with severe AIP co-treated with DSS and poly (I:C). The degree of experimental AIP, but not of autoimmune sialadenitis, was greater in germ-free mice mono-colonized with S. sciuri and treated with poly (I:C) than in germ-free mice treated with poly (I:C) alone, which was accompanied by the increased accumulation of IFN-α- and IL-33-producing pDCs. Taken together, these data suggest that intestinal barrier dysfunction exacerbates AIP through the activation of pDCs and translocation of S. sciuri into the pancreas.</jats:p>
収録刊行物
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- International Immunology
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International Immunology 34 (12), 621-634, 2022-09-01
Oxford University Press (OUP)