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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
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Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
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Increased ACE2 and TMPRSS2 expression in ulcerative colitis.

Yuichiro Hamamoto1, Michihiro Kawamura2, Hiroki Uchida2

  • 1Department of Diagnostic Pathology, Kinki Central Hospital, Itami, Hyogo, Japan; Department of Pathology, Osaka University Graduate School of Medicine, Suita, Japan.

Pathology, Research and Practice
|January 21, 2024
PubMed
Summary
This summary is machine-generated.

This study found increased expression of ACE2 and TMPRSS2 in ulcerative colitis (UC) patients, suggesting these SARS-CoV-2 entry molecules may play a role in UC pathogenesis.

Keywords:
ACE2COVID-19Inflammatory bowel diseaseSARS-CoV-2TMPRSS2Ulcerative colitis

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Area of Science:

  • Gastroenterology
  • Immunology
  • Virology

Background:

  • Ulcerative colitis (UC) is an inflammatory bowel disease with unclear pathogenesis.
  • Angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) are key entry molecules for SARS-CoV-2.
  • Previous reports suggest a potential association between ACE2, TMPRSS2, and UC, but consensus is lacking.

Purpose of the Study:

  • To investigate the expression levels of ACE2 and TMPRSS2 in colorectal tissues of patients with ulcerative colitis.
  • To determine if ACE2 and TMPRSS2 expression in UC is influenced by the COVID-19 pandemic.

Main Methods:

  • Colorectal specimens were collected from 60 individuals (30 UC patients, 30 controls) between 2018 and 2021.
  • Immunohistochemistry was employed to analyze the proportion and intensity of ACE2 and TMPRSS2 expression.
  • Statistical analysis was performed to compare expression levels between UC patients and controls.

Main Results:

  • A significant increase in the proportion of ACE2 expression was observed in UC patients compared to controls.
  • A significant increase in the intensity of TMPRSS2 expression was found in UC patients.
  • Expression levels of ACE2 and TMPRSS2 in UC were not affected by the COVID-19 pandemic.

Conclusions:

  • ACE2 and TMPRSS2 are upregulated in the colon and rectum of ulcerative colitis patients.
  • These findings suggest a potential role for ACE2 and TMPRSS2 in the pathogenesis of ulcerative colitis.
  • Further research is warranted to elucidate the specific mechanisms involved.