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Published on: October 5, 2012
The Bcl-2/Bax system and apoptosis in ulcerative colitis
D G Karamanolis1, Ioannis Kyrlagkitsis, K Konstantinou
1Department of Gastroenterology, Tzanio Hospital, Pireas, Greece.
Hepato-Gastroenterology
|July 17, 2007
Summary
This study investigated apoptosis in ulcerative colitis (UC), finding Bcl-2, Bax, and Bcl-x were upregulated in patients. However, severe UC showed downregulation of Bax and Bcl-x, suggesting complex roles in UC pathogenesis.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory colon disease with unknown causes.
- Apoptosis (programmed cell death) is implicated in UC pathogenesis.
- The roles of Bcl-2, Bax, and Bcl-x proteins in UC apoptosis require further elucidation.
Purpose of the Study:
- To prospectively determine the involvement of Bcl-2, Bax, and Bcl-x in the apoptotic pathway of ulcerative colitis.
- To correlate the expression of these proteins with disease severity and apoptosis levels in UC patients.
Main Methods:
- A prospective study included 23 UC patients and 11 controls.
- Histological severity was assessed using the Sidney classification.
- In situ apoptosis was evaluated by TUNEL assay; Bax, Bcl-2, and Bcl-x expression by immunohistochemistry; and cellular proliferation by Ki67 staining.
Main Results:
- Bcl-2, Bax, and Bcl-x were upregulated in UC patients compared to controls.
- Moderate/severe UC showed downregulation of Bax in epithelial cells and Bcl-x in lymphocytes.
- Weak correlations were observed between epithelial apoptosis and Bcl-x/Bax expression in lymphocytes.
Conclusions:
- The Bcl-2/Bax system does not seem to directly induce apoptosis in ulcerative colitis.
- Activation of intraepithelial lymphocytes may be linked to epithelial apoptosis or be a consequence of inflammation in UC.
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