Tu1700 Increased Abundance of Bacteria Producing Hydrogen Sulfide in the Colonic Mucosa of Patients With Ulcerative Colitis and Crohn's Disease

Background—The pathogenesis of ulcerative colitis is unclear, but cytotoxic T lymphocytes infiltrating the mucosa have been implicated in mucosal damage. The Fas ligand (FasL), expressed on cytotoxic T lymphocytes, induces apoptosis in cells expressing Fas.Aim—To analyse FasL expression in affected colonic mucosa to ascertain Fas-FasL interaction in ulcerative colitis.Methods—FasL mRNA was quantified in colonic mucosal specimens from healthy subjects and patients with ulcerative colitis or Crohn’s disease, using the competitive reverse transcription polymerase chain reaction. FasL mRNA localisation was determined by in situ hybridisation. Expression of Fas in colonic mucosa was analysed immunohistochemically. Phenotypes of lamina propria lymphocytes that expressed FasL were analysed by flow cytometry.Results—FasL mRNA was strongly expressed in active ulcerative colitis lesions, but not in those associated with active Crohn’s disease or active proctitis-type ulcerative colitis. In situ hybridisation showed that FasL mRNA expression occurred in mononuclear cells infiltrating lesions. Fas was expressed in epithelial cells in ulcerative colitis and Crohn’s disease, and in normal subjects. Cytometry showed that FasL was expressed in CD3 lymphocytes infiltrating the lamina propria in active lesions.Conclusions—FasL is expressed in CD3 lymphocytes infiltrating into ulcerative colitis but not Crohn’s disease lesions, suggesting that Fas-FasL induced apoptosis participates in the mucosal damage of ulcerative colitis.

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T-cell immune response against cytomegalovirus in peripheral blood and colonic mucosa from ulcerative colitis and Crohn's disease patients

Intestinal Research ◽

10.5217/ir.2018.16.1.160 ◽

2018 ◽

Vol 16 (1) ◽

pp. 160

Author(s):

Seung-Joo Nam ◽

Eun Sun Kim ◽

Yoon Tae Jeen

Keyword(s):

Ulcerative Colitis ◽

Immune Response ◽

Crohn’S Disease ◽

T Cell ◽

Crohn's Disease ◽

Peripheral Blood ◽

Colonic Mucosa ◽

Cell Immune Response

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Delineating cytokine signaling pathways in ulcerative colitis and Crohn's disease through colonic mucosa gene expression profiles.

Inflammatory Bowel Diseases ◽

10.1093/ibd/17.supplement1.s21a ◽

2011 ◽

Vol 17 (suppl_1) ◽

pp. S21-S21

Author(s):

G Christophi ◽

R Rong ◽

P Massa ◽

P Holtzapple ◽

S Landas

Keyword(s):

Gene Expression ◽

Ulcerative Colitis ◽

Crohn’S Disease ◽

Crohn's Disease ◽

Signaling Pathways ◽

Colonic Mucosa ◽

Expression Profiles ◽

Gene Expression Profiles ◽

Cytokine Signaling

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Substrate utilization by intestinal mucosal tissue strips from patients with inflammatory bowel disease

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.281.2.g405 ◽

2001 ◽

Vol 281 (2) ◽

pp. G405-G411 ◽

Cited By ~ 12

Author(s):

Jimmy Jørgensen ◽

Per Brøbech Mortensen

Keyword(s):

Ulcerative Colitis ◽

Inflammatory Bowel Disease ◽

Crohn’S Disease ◽

Crohn's Disease ◽

Bowel Disease ◽

Metabolic Disorder ◽

Colonic Mucosa ◽

Ketone Bodies ◽

Inflammatory Bowel ◽

Small Intestinal

A primary metabolic disorder may be present in the colonic mucosa of patients with ulcerative colitis. Preserving the epithelium in situ, we evaluated the metabolism of the colonic mucosa of control patients and patients with ulcerative colitis and Crohn's disease. Colonic mucosal strips (∼500 mg) were incubated with partially14C-labeled acetate (C2), butyrate (C4), hexanoate (C6), octanoate (C8), and glucose, and the production of CO2and ketone bodies was quantitated. Metabolism by small intestinal mucosal strips was also evaluated. Compared with controls, no decrease in either CO2or ketone body production by colonic strips from patients with either ulcerative colitis or Crohn's disease was observed for any substrate. The CO2production from each of the C2–C8fatty acids was the same for colonic and small intestinal strips, whereas CO2production from glucose was higher in small intestinal strips than in colonic strips. The production of ketone bodies was low in small intestinal strips. A primary metabolic disorder in the colonic mucosa of patients with inflammatory bowel disease was not found.

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