Journal
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 84, Issue 10, Pages 1043-1050Publisher
NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS
DOI: 10.1139/Y06-056
Keywords
epithelial apoptosis; lipopolysaccharide; caspase-3; permeability; ZO-l
Categories
Ask authors/readers for more resources
The mechanisms responsible for microbially induced epithelial apoptosis and increased intestinal permeability remain unclear. This Study assessed whether Purified bacterial lipopolysaccharide (LPS) increases epithelial apoptosis and permeability and whether these changes are dependent on caspase-3 activation. In nontumorigenic epithelial monolayers, Escherichia coli O26:B6 LPS increased apoptosis, as shown by nuclear breakdown, caspase-3 activation, and PARP cleavage, and induced disruption Of tight junctional ZO-1. Apical, but not basolateral, exposure to LPS increased epithelial permeability. Addition of a caspase-3 inhibitor abolished the effects of LPS. The findings describe a novel mechanism whereby apical LPS may disrupt epithelial tight junctional ZO-1 and barrier function in a caspase-3-dependent fashion.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available