期刊
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
卷 84, 期 10, 页码 1043-1050出版社
NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS
DOI: 10.1139/Y06-056
关键词
epithelial apoptosis; lipopolysaccharide; caspase-3; permeability; ZO-l
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.
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