Ultrastructural changes in colonic epithelial cells in a rat model of inflammatory bowel disease

Abstract

Inflammatory bowel disease (IBD) is a global, chronic intractable disease. The functions of drugs and food components have been evaluated in models of IBD induced by 2,4,6‐trinitrobenzene sulfonic acid (TNBS). Here, we used transmission (TEM) and osmium‐maceration scanning (SEM) electron microscopy to evaluate the ultrastructure of colonic epithelial cells in rat models of IBD induced by TNBS. Histological evaluation revealed that the intestinal crypts in the most regions of the IBD‐model colons were deformed and we classified them as having high cell migration rates (HMIG). The remaining regions in the intestinal crypts retained a relatively normal structure and we classified them as having low cell migration rates (LMIG). Osmium‐maceration SEM revealed the mucosal fluid flowing in spaces without secretory granules in crypt goblet cells of both HMIG and LMIG regions, indicating the depletion of goblet cell mucin that is found in patients with IBD. The Golgi apparatus in absorptive cells was stacked and curled in both regions. Osmium‐maceration SEM showed membrane network structures resembling endoplasmic reticulum that were large and expanded in absorptive cells with HMIG rather than with LMIG regions in IBD‐model colons. These findings indicated that endoplasmic reticulum stress is associated with susceptibility to IBD and that the effects of various agents can be evaluated according to endoplasmic reticulum stress revealed by using electron microscopy in models of IBD induced by TNBS.

Ultrastructural changes in chronic inflammatory enteropathies—a comparison between dogs and humans

“…The intestinal epithelial cell ultrastructure was also altered in experimental rodent models of IBD ( Pfeiffer et al, 1997 ; Tian et al, 2003 ; Bou-Fersen et al, 2008 ; Bochimoto et al, 2019 ). The colonic ultrastructure in a 2,4,6-trinitrobenzene sulfonic acid (TNBSA)-induced IBD/colitis model, for example, revealed a mixed picture of deformed intestinal crypt areas with high cell migration rates and a more regular structure with low cell migration rates in the remaining intestinal crypts ( Bochimoto et al, 2019 ).…”

“…The intestinal epithelial cell ultrastructure was also altered in experimental rodent models of IBD ( Pfeiffer et al, 1997 ; Tian et al, 2003 ; Bou-Fersen et al, 2008 ; Bochimoto et al, 2019 ). The colonic ultrastructure in a 2,4,6-trinitrobenzene sulfonic acid (TNBSA)-induced IBD/colitis model, for example, revealed a mixed picture of deformed intestinal crypt areas with high cell migration rates and a more regular structure with low cell migration rates in the remaining intestinal crypts ( Bochimoto et al, 2019 ). The depletion of goblet cell mucin, stacked to curled Golgi apparatus in absorptive cells, and remnants of the ER support that ER stress plays an important role in the pathogenesis of IBD ( Bochimoto et al, 2019 ).…”