Open AccessEffect of Helicobacter pylori infection on the link between GLP-1 expression and motility of the gastrointestinal tract
Author(s) -
Hirotsugu Eda,
Hirokazu Fukui,
Ryosuke Uchiyama,
Yoshitaka Kitayama,
Ken Hara,
Mo Yang,
Mio Kodani,
Toshihiko Tomita,
Tadayuki Oshima,
Jiro Watari,
Hiroko Tsutsui,
Hiroto Miwa
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0177232
Subject(s) - helicobacter pylori , motility , gastrointestinal tract , medicine , immunohistochemistry , gastroenterology , stomach , biology , genetics
Background Although Helicobacter pylori ( H . pylori ) infection is closely associated with the development of peptic ulcer, its involvement in pathophysiology in the lower intestinal tract and gastrointestinal (GI) motility remains unclear. Glucagon-like peptide-1 (GLP-1) is a gut hormone produced in the lower intestinal tract and involved in GI motility. Here, we investigated the effect of H . pylori infection on the link between GLP-1 expression and motility of the GI tract. Methods C57BL/6 mice were inoculated with a H . pylori strain. Twelve weeks later, the H . pylori -infected mice underwent H . pylori eradication treatment. GI tissues were obtained from the mice at various time intervals, and evaluated for the severity of gastric inflammatory cell infiltration and immunohistochemical expression of GLP-1 and PAX6 in the colonic mucosa. Gastrointestinal transit time (GITT) was measured by administration of carmine-red solution. Results GLP-1 was expressed in the endocrine cells of the colonic mucosa, and PAX6 immunoreactivity was co-localized in such cells. The numbers of GLP-1- and PAX6-positive cells in the colon were significantly increased at 12 weeks after H . pylori infection and showed a positive correlation with each other. The GITT was significantly longer in H . pylori -infected mice than in non-infected controls and showed a positive correlation with GLP-1 expression. When H . pylori -infected mice underwent H . pylori eradication, GITT and PAX6/GLP-1 expression did not differ significantly from those in untreated H . pylori -infected mice. Conclusions H . pylori infection may impair GI motility by enhancing the colonic GLP-1/PAX6 expression.