Гомосексуальный субъект в пространстве публичного: нарративное измерение камин-аута

<div><p>Background</p><p>Although <i>Helicobacter pylori</i> (<i>H</i>. <i>pylori</i>) 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 <i>H</i>. <i>pylori</i> infection on the link between GLP-1 expression and motility of the GI tract.</p><p>Methods</p><p>C57BL/6 mice were inoculated with a <i>H</i>. <i>pylori</i> strain. Twelve weeks later, the <i>H</i>. <i>pylori</i>-infected mice underwent <i>H</i>. <i>pylori</i> 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.</p><p>Results</p><p>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 <i>H</i>. <i>pylori</i> infection and showed a positive correlation with each other. The GITT was significantly longer in <i>H</i>. <i>pylori</i>-infected mice than in non-infected controls and showed a positive correlation with GLP-1 expression. When <i>H</i>. <i>pylori</i>-infected mice underwent <i>H</i>. <i>pylori</i> eradication, GITT and PAX6/GLP-1 expression did not differ significantly from those in untreated <i>H</i>. <i>pylori</i>-infected mice.</p><p>Conclusions</p><p><i>H</i>. <i>pylori</i> infection may impair GI motility by enhancing the colonic GLP-1/PAX6 expression.</p></div