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We have previously reported that innate immune activation contributes to the development of AIP and IgG4-RD, as these diseases are characterized by the production of IFN-\u03b1 and IL-33 by plasmacytoid dendritic cells (pDCs) that mediate chronic fibroinflammatory responses. In this study, we investigated the roles played by innate immunity against intestinal microflora in experimental AIP induced in MRL\/MpJ mice by repeated administrations of 100 \u00b5g of polyinosinic-polycytidylic acid [poly (I:C)]. Bowel sterilization with a broad spectrum of antibiotics inhibited pancreatic accumulation of pDCs producing IFN-\u03b1 and IL-33, and thereby suppressed the development of AIP. Mice treated with 10 \u00b5g of poly (I:C) developed severe AIP equivalent to that induced by 100 \u00b5g of poly (I:C) upon co-housing with mice treated with 100 \u00b5g of poly (I:C). Fecal microbiota transplantation (FMT) from donor mice treated with 100 \u00b5g of poly (I:C) led to the development of severe AIP in the recipient mice upon injection with 10 \u00b5g of poly (I:C). Induction of severe AIP in mice with 10 \u00b5g of poly (I:C) was associated with pancreatic accumulation of pDCs producing IFN-\u03b1 and IL-33 in the co-housing and FMT experiments. These data collectively suggest that innate immune responses against intestinal microflora are involved in the development of experimental AIP, and that intestinal dysbiosis increases sensitivity to experimental AIP via activation of pDCs.<\/jats:p>","DOI":"10.1093\/intimm\/dxz050","type":"journal-article","created":{"date-parts":[[2019,6,27]],"date-time":"2019-06-27T19:10:28Z","timestamp":1561662628000},"page":"795-809","source":"Crossref","is-referenced-by-count":48,"title":["Intestinal dysbiosis mediates experimental autoimmune pancreatitis via activation of plasmacytoid dendritic cells"],"prefix":"10.1093","volume":"31","author":[{"given":"Ken","family":"Kamata","sequence":"first","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomohiro","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kosuke","family":"Minaga","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akane","family":"Hara","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoe","family":"Yoshikawa","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayana","family":"Okamoto","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kentaro","family":"Yamao","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mamoru","family":"Takenaka","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ah-Mee","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masatoshi","family":"Kudo","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine , Osaka-Sayama, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,7,9]]},"reference":[{"key":"2022071007555961100_CIT0001","doi-asserted-by":"crossref","first-page":"874","DOI":"10.1016\/j.it.2018.09.005","article-title":"Mechanistic insights into autoimmune pancreatitis and IgG4-related disease","volume":"39","author":"Watanabe","year":"2018","journal-title":"Trends Immunol"},{"key":"2022071007555961100_CIT0002","doi-asserted-by":"crossref","first-page":"1373","DOI":"10.1136\/gutjnl-2012-304224","article-title":"Recent advances in autoimmune pancreatitis: type 1 and type 2","volume":"62","author":"Kamisawa","year":"2013","journal-title":"Gut"},{"key":"2022071007555961100_CIT0003","doi-asserted-by":"crossref","first-page":"613","DOI":"10.1007\/s00535-006-1862-6","article-title":"Autoimmune pancreatitis: proposal of IgG4-related sclerosing disease","volume":"41","author":"Kamisawa","year":"2006","journal-title":"J. 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