Pancreatic glycoprotein 2 is a first line of defense for mucosal protection in intestinal inflammation

Author:

Kurashima Yosuke,Kigoshi TakaakiORCID,Murasaki Sayuri,Arai Fujimi,Shimada Kaoru,Seki Natsumi,Kim Yun-Gi,Hase KojiORCID,Ohno HiroshiORCID,Kawano Kazuya,Ashida Hiroshi,Suzuki Toshihiko,Morimoto Masako,Saito Yukari,Sasou Ai,Goda Yuki,Yuki Yoshikazu,Inagaki YutakaORCID,Iijima Hideki,Suda Wataru,Hattori Masahira,Kiyono HiroshiORCID

Abstract

AbstractIncreases in adhesive and invasive commensal bacteria, such as Escherichia coli, and subsequent disruption of the epithelial barrier is implicated in the pathogenesis of inflammatory bowel disease (IBD). However, the protective systems against such barrier disruption are not fully understood. Here, we show that secretion of luminal glycoprotein 2 (GP2) from pancreatic acinar cells is induced in a TNF–dependent manner in mice with chemically induced colitis. Fecal GP2 concentration is also increased in Crohn’s diease patients. Furthermore, pancreas-specific GP2-deficient colitis mice have more severe intestinal inflammation and a larger mucosal E. coli population than do intact mice, indicating that digestive-tract GP2 binds commensal E. coli, preventing epithelial attachment and penetration. Thus, the pancreas–intestinal barrier axis and pancreatic GP2 are important as a first line of defense against adhesive and invasive commensal bacteria during intestinal inflammation.

Funder

Japan Agency for Medical Research and Development

MEXT | Japan Society for the Promotion of Science

Publisher

Springer Science and Business Media LLC

Subject

General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry

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