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The UspA1 protein of Moraxella catarrhalis induces CEACAM-1-dependent apoptosis in alveolar epithelial cells.

N'Guessan, PD. (author)
Vigelahn, M. (author)
Bachmann, S. (author)
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Zabel, S. (author)
Opitz, B. (author)
Schmeck, B. (author)
Hippenstiel, S. (author)
Zweigner, J. (author)
Riesbeck, Kristian (author)
Lund University,Lunds universitet,Klinisk mikrobiologi, Malmö,Forskargrupper vid Lunds universitet,Clinical Microbiology, Malmö,Lund University Research Groups
Singer, BB. (author)
Suttorp, N. (author)
Slevogt, H. (author)
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 (creator_code:org_t)
Oxford University Press (OUP), 2007
2007
English.
In: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 195:11, s. 1651-1660
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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 headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Mikrobiologi inom det medicinska området (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Microbiology in the medical area (hsv//eng)

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