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Moraxella catarrhalis induces an immune response in the murine lung which is independent of human CEACAM5 expression and long-term smoke exposure.

Gutbier, Birgitt; Fischer, Katja; Doehn, Jan-Moritz; von Lachner, Carolin; Herr, Christian; Klaile, Esther; Frischmann, Ursula; Singer, Bernhard B; Riesbeck, Kristian LU and Zimmermann, Wolfgang, et al. (2015) In American Journal of Physiology: Lung Cellular and Molecular Physiology 309(3). p.250-261
Abstract
In patients with chronic obstructive pulmonary disease (COPD), Moraxella catarrhalis infection of the lower airways is associated with chronic colonization and inflammation during stable disease and acute exacerbations. Chronic smoke exposure induces chronic inflammation and impairs mucociliary clearance, thus contributing to bacterial colonization of the lower airways in COPD patients. The human-specific carcinoembryonic antigen-related cell adhesion molecule (CEACAM) 5, expressed in human airways, has been shown to contribute to epithelial colonization of CEACAM-binding pathogens. To investigate the impact of CEACAM5 expression on pulmonary M. catarrhalis colonization, we infected mice transgenic for human CEACAM5 (hCEACAM5) and wild... (More)
In patients with chronic obstructive pulmonary disease (COPD), Moraxella catarrhalis infection of the lower airways is associated with chronic colonization and inflammation during stable disease and acute exacerbations. Chronic smoke exposure induces chronic inflammation and impairs mucociliary clearance, thus contributing to bacterial colonization of the lower airways in COPD patients. The human-specific carcinoembryonic antigen-related cell adhesion molecule (CEACAM) 5, expressed in human airways, has been shown to contribute to epithelial colonization of CEACAM-binding pathogens. To investigate the impact of CEACAM5 expression on pulmonary M. catarrhalis colonization, we infected mice transgenic for human CEACAM5 (hCEACAM5) and wild type mice intratracheally with M. catarrhalis with or without preceding smoke exposure and analyzed bacterial colonization and local and systemic inflammation. Our results show that airway infection with M. catarrhalis accelerated acute local but not systemic inflammation, albeit independent of hCEACAM5 expression. Long-term smoke exposure alone or prior to M. catarrhalis infection did not contribute to increased local or systemic inflammation. No difference was found in pulmonary clearance of M. catarrhalis in hCEACAM5-transgenic mice compared to wild type mice. Smoke exposure neither altered time nor extent of persistence of M. catarrhalis in the lungs of both genotypes. In conclusion, M. catarrhalis induced a local acute immune response in murine airways. Neither hCEACAM5- expression nor chronic smoke exposure nor a combination of both was sufficient as prerequisites for the establishment of chronic M. catarrhalis colonization. Our results demonstrate the difficulties in mirroring conditions of chronic airways colonization of M. catarrhalis in a murine model. (Less)
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American Journal of Physiology: Lung Cellular and Molecular Physiology
volume
309
issue
3
pages
250 - 261
publisher
American Physiological Society
external identifiers
  • pmid:26047639
  • wos:000358945600005
  • scopus:84938651143
ISSN
1522-1504
DOI
10.1152/ajplung.00265.2014
language
English
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yes
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3a627ce7-7c73-4b06-9917-0a5681167e70 (old id 7488067)
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http://www.ncbi.nlm.nih.gov/pubmed/26047639?dopt=Abstract
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2015-07-06 16:17:41
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2017-08-06 03:25:28
@article{3a627ce7-7c73-4b06-9917-0a5681167e70,
  abstract     = {In patients with chronic obstructive pulmonary disease (COPD), Moraxella catarrhalis infection of the lower airways is associated with chronic colonization and inflammation during stable disease and acute exacerbations. Chronic smoke exposure induces chronic inflammation and impairs mucociliary clearance, thus contributing to bacterial colonization of the lower airways in COPD patients. The human-specific carcinoembryonic antigen-related cell adhesion molecule (CEACAM) 5, expressed in human airways, has been shown to contribute to epithelial colonization of CEACAM-binding pathogens. To investigate the impact of CEACAM5 expression on pulmonary M. catarrhalis colonization, we infected mice transgenic for human CEACAM5 (hCEACAM5) and wild type mice intratracheally with M. catarrhalis with or without preceding smoke exposure and analyzed bacterial colonization and local and systemic inflammation. Our results show that airway infection with M. catarrhalis accelerated acute local but not systemic inflammation, albeit independent of hCEACAM5 expression. Long-term smoke exposure alone or prior to M. catarrhalis infection did not contribute to increased local or systemic inflammation. No difference was found in pulmonary clearance of M. catarrhalis in hCEACAM5-transgenic mice compared to wild type mice. Smoke exposure neither altered time nor extent of persistence of M. catarrhalis in the lungs of both genotypes. In conclusion, M. catarrhalis induced a local acute immune response in murine airways. Neither hCEACAM5- expression nor chronic smoke exposure nor a combination of both was sufficient as prerequisites for the establishment of chronic M. catarrhalis colonization. Our results demonstrate the difficulties in mirroring conditions of chronic airways colonization of M. catarrhalis in a murine model.},
  author       = {Gutbier, Birgitt and Fischer, Katja and Doehn, Jan-Moritz and von Lachner, Carolin and Herr, Christian and Klaile, Esther and Frischmann, Ursula and Singer, Bernhard B and Riesbeck, Kristian and Zimmermann, Wolfgang and Suttorp, Norbert and Bachmann, Sebastian and Bals, Robert and Witzenrath, Martin and Slevogt, Hortense},
  issn         = {1522-1504},
  language     = {eng},
  number       = {3},
  pages        = {250--261},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Lung Cellular and Molecular Physiology},
  title        = {Moraxella catarrhalis induces an immune response in the murine lung which is independent of human CEACAM5 expression and long-term smoke exposure.},
  url          = {http://dx.doi.org/10.1152/ajplung.00265.2014},
  volume       = {309},
  year         = {2015},
}