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

N'Guessan, PD.; Vigelahn, M.; Bachmann, S.; Zabel, S.; Opitz, B.; Schmeck, B.; Hippenstiel, S.; Zweigner, J.; Riesbeck, Kristian LU and Singer, BB., et al. (2007) In Journal of Infectious Diseases 195(11). p.1651-1660
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.... (More)
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. (Less)
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publication status
published
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Journal of Infectious Diseases
volume
195
issue
11
pages
1651 - 1660
publisher
Oxford University Press
external identifiers
  • Scopus:34249086216
ISSN
1537-6613
DOI
10.1086/514820
language
English
LU publication?
yes
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a7f357e4-c6d3-4569-bf2f-386df3d03ced (old id 1142521)
date added to LUP
2008-08-07 10:22:44
date last changed
2016-10-13 04:47:12
@misc{a7f357e4-c6d3-4569-bf2f-386df3d03ced,
  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.},
  author       = {N'Guessan, PD. and Vigelahn, M. and Bachmann, S. and Zabel, S. and Opitz, B. and Schmeck, B. and Hippenstiel, S. and Zweigner, J. and Riesbeck, Kristian and Singer, BB. and Suttorp, N. and Slevogt, H.},
  issn         = {1537-6613},
  language     = {eng},
  number       = {11},
  pages        = {1651--1660},
  publisher    = {ARRAY(0xba6faf0)},
  series       = {Journal of Infectious Diseases},
  title        = {The UspA1 protein of Moraxella catarrhalis induces CEACAM-1-dependent apoptosis in alveolar epithelial cells.},
  url          = {http://dx.doi.org/10.1086/514820},
  volume       = {195},
  year         = {2007},
}