Dislocation of tight junction proteins without F-actin disruption in inactive Crohn's disease

  • Authors:
    • Nobuhide Oshitani
    • Kenji Watanabe
    • Shiro Nakamura
    • Yasuhiro Fujiwara
    • Kazuhide Higuchi
    • Tetsuo Arakawa
  • View Affiliations

  • Published online on: March 1, 2005     https://doi.org/10.3892/ijmm.15.3.407
  • Pages: 407-410
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Abstract

Crohn's disease is associated with increased permeability of the intestinal barrier even in quiescent patients. Increased intestinal permeability may cause dysregulated immunological responses in the intestinal mucosa that leads to chronic intestinal inflammation. We have studied the expression of tight junction proteins (occludin and zonula occludens), α2-smooth muscle actin, TGF-β with a cytoskeletal protein (F-actin) in the intestinal epithelium of patients with inflammatory bowel disease. Surgical samples were obtained from 6 controls (individuals without inflammatory bowel disease), 8 patients with ulcerative colitis and 7 patients with Crohn's disease. F-actin was visualized with fluorescein phalloidin. Tight junction proteins, α2 smooth muscle actin, and TGFβ were visualized by the immunofluorescent method. Occludin and zonula occludens found in apical tight junctions in normal epithelium were dislocated to the basolateral position and in the lamina propria extracellular matrix in patients with Crohn's disease, while the structure of F-actin was maintained in inactive or minimally inflamed mucosa. TGF-β positive inflammatory cells were increased in ulcerative colitis and Crohn's disease mucosa. Subepithelial myofibroblasts were constitutively found in controls, ulcerative colitis, and Crohn's disease mucosa. Latent dislocation of tight junction proteins, without disturbance of the cytoskeleton in the inactive mucosa of patients with Crohn's disease, may permit the invasion of gut antigens because the functional disruption of tight junctions could initiate an altered immune response.

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March 2005
Volume 15 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Oshitani N, Watanabe K, Nakamura S, Fujiwara Y, Higuchi K and Arakawa T: Dislocation of tight junction proteins without F-actin disruption in inactive Crohn's disease. Int J Mol Med 15: 407-410, 2005
APA
Oshitani, N., Watanabe, K., Nakamura, S., Fujiwara, Y., Higuchi, K., & Arakawa, T. (2005). Dislocation of tight junction proteins without F-actin disruption in inactive Crohn's disease. International Journal of Molecular Medicine, 15, 407-410. https://doi.org/10.3892/ijmm.15.3.407
MLA
Oshitani, N., Watanabe, K., Nakamura, S., Fujiwara, Y., Higuchi, K., Arakawa, T."Dislocation of tight junction proteins without F-actin disruption in inactive Crohn's disease". International Journal of Molecular Medicine 15.3 (2005): 407-410.
Chicago
Oshitani, N., Watanabe, K., Nakamura, S., Fujiwara, Y., Higuchi, K., Arakawa, T."Dislocation of tight junction proteins without F-actin disruption in inactive Crohn's disease". International Journal of Molecular Medicine 15, no. 3 (2005): 407-410. https://doi.org/10.3892/ijmm.15.3.407