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

Quantitative evaluation of GLP-1 expression in the colon of mice infected with <i>H</i>. <i>pylori</i> and after <i>H</i>. <i>pylori</i> eradication.

<p>Results are expressed as the mean ± SEM (n = 5). *Significantly different between two groups; <i>P</i> < 0.05.</p

Effect of <i>H</i>. <i>pylori</i> infection on gastric inflammatory cell infiltration and colonic GLP-1 expression.

<p>(A) Representative images of GI tissues in mice with <i>H</i>. <i>pylori</i> infection. Inflammatory cells are mainly infiltrating into the mucosal lamina propria in the stomach. GLP-1 is expressed in the cytoplasm of ovoid or pyramidal epithelial cells in the colonic mucosa and the number of these cells is increased relative to control mice without <i>H</i>. <i>pylori</i> infection. (B) Serial scores of inflammatory cell infiltration in the gastric mucosa of mice with <i>H</i>. <i>pylori</i> infection. (C) Serial counts of GLP-1-positive cells in the colonic mucosa of mice with <i>H</i>. <i>pylori</i> infection. (D) Correlation between scores for gastric inflammatory cell infiltration and number of colonic GLP-1-posiitve cells. ○, control without <i>H</i>. <i>pylori</i> infection; ●, <i>H</i>. <i>pylori</i>-infected mice. All the results are expressed as the mean ± SE. Significantly greater than control at start of the experiment: *<i>P</i> <0.05.</p

Effect of <i>H</i>. <i>pylori</i> infection on colonic PAX6 expression.

<p>(A) Immunostaining of PAX6 in the colonic mucosa of mice with <i>H</i>. <i>pylori</i> infection. PAX6 is expressed in the nuclei of colonic epithelial cells (arrows) and the number of cells expressing it is increased relative to control mice without <i>H</i>. <i>pylori</i> infection. Double immunostaining showing co-expression of GLP-1 (green) and PAX6 (red) in a colonic epithelial cell. (B) Serial counts of PAX6-posiitve cells in the colonic mucosa of mice with <i>H</i>. <i>pylori</i> infection. (C) Correlation between the numbers of PAX6- and GLP-1-positive cells. ○, control without <i>H</i>. <i>pylori</i> infection; ●, <i>H</i>. <i>pylori</i>-infected mice. All the results are expressed as the mean ± SE. Significantly greater than control at start of the experiment: *<i>P</i> <0.05.</p

Effect of <i>H</i>. <i>pylori</i> infection and its eradication on GI motility.

<p>(A) Histology of the gastric mucosa in mice with <i>H</i>. <i>pylori</i> infection and after eradication. When compared with untreated mice with <i>H</i>. <i>pylori</i> infection, the inflammatory cell infiltration is clearly suppressed in mice after eradication treatment. (B) Scores of inflammatory cell infiltration in the gastric mucosa of mice infected with <i>H</i>. <i>pylori</i>, and after <i>H</i>. <i>pylori</i> eradication. Mean values are shown as bars. (C) Gastrointestinal transit time in mice infected with <i>H</i>. <i>pylori</i> and after <i>H</i>. <i>pylori</i> eradication. Data are presented as medians and interquartile range (n = 5 in each group). Significantly different between two groups: *<i>P</i> <0.05. NS, not significant.</p