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J Infect Dis ; 195(11): 1651-60, 2007 Jun 01.
Article in English | MEDLINE | ID: mdl-17471435

ABSTRACT

Moraxella catarrhalis is a major cause of exacerbations of chronic obstructive pulmonary disease (COPD) and emphysema. M. catarrhalis-specific UspA1 and the epithelial carcinoembryonic antigen-related cell adhesion molecule (CEACAM1) were required to induce apoptosis. M. catarrhalis-induced apoptosis was significantly enhanced in HeLa cells stably transfected with CEACAM1, compared with HeLa cells not expressing CEACAM1. Infected cells showed increased activity of caspases 3, 6, and 9 but not of caspase 8. Reduced expression of Bcl-2, translocation of Bax into the mitochondria, and cytosolic increase of apoptosis-inducing factor in M. catarrhalis-infected cells implicated the involvement of mitochondrial death pathways. In conclusion, M. catarrhalis induced apoptosis in pulmonary epithelial cells--a process that was triggered by interaction between CEACAM1 and UspA1. Thus, M. catarrhalis-induced apoptosis of pulmonary epithelial cells may contribute to the development of COPD and emphysema.


Subject(s)
Antigens, CD/metabolism , Apoptosis/physiology , Bacterial Outer Membrane Proteins/metabolism , Cell Adhesion Molecules/metabolism , Epithelial Cells/microbiology , Moraxella catarrhalis/pathogenicity , Pulmonary Alveoli/microbiology , Cell Line , HeLa Cells , Humans , Moraxella catarrhalis/metabolism , Pulmonary Alveoli/cytology
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