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Ultrastructure of intestinal mucosa in diarrhea-predominant irritable bowel syndrome.

Authors :
Zhao DY
Qi QQ
Long X
Li X
Chen FX
Yu YB
Zuo XL
Source :
Physiology international [Physiol Int] 2019 Sep 01; Vol. 106 (3), pp. 225-235. Date of Electronic Publication: 2019 Sep 27.
Publication Year :
2019

Abstract

Objectives: Impaired intestinal barrier function has been demonstrated in the pathophysiology of diarrhea-predominant irritable bowel syndrome (IBS-D). This study aimed to describe the intestinal ultrastructural findings in the intestinal mucosal layer of IBS-D patients.<br />Methods: In total, 10 healthy controls and 10 IBS-D patients were analyzed in this study. The mucosa of each patient's rectosigmoid colon was first assessed by confocal laser endomicroscopy (CLE); next, biopsied specimens of these sites were obtained. Intestinal tissues of IBS-D patients and healthy volunteers were examined to observe cellular changes by transmission electron microscopy (TEM).<br />Results: CLE showed no visible epithelial damage or inflammatory changes in the colonic mucosa of IBS-D compared with healthy volunteers. On transmission electron microscopic examination, patients with IBS-D displayed a larger apical intercellular distance with a higher proportion of dilated (>20 nm) intercellular junctional complexes, which was indicative of impaired mucosal integrity. In addition, microvillus exfoliation, extracellular vesicle as well as increased presence of multivesicular bodies were visible in IBS-D patients. Single epithelial cells appeared necrotic, as characterized by cytoplasmic vacuolization, cytoplasmic swelling, and presence of autolysosome. A significant association between bowel habit, frequency of abdominal pain, and enlarged intercellular distance was found.<br />Conclusion: This study showed ultrastructural alterations in the architecture of intestinal epithelial cells and intercellular junctional complexes in IBS-D patients, potentially representing a pathophysiological mechanism in IBS-D.

Details

Language :
English
ISSN :
2498-602X
Volume :
106
Issue :
3
Database :
MEDLINE
Journal :
Physiology international
Publication Type :
Academic Journal
Accession number :
31560236
Full Text :
https://doi.org/10.1556/2060.106.2019.20