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Streptococcus pneumoniae induces expression of the antibacterial CXC chemokine MIG/CXCL9 via MyD88-dependent signaling in a murine model of airway infection.

Abstract
MIG/CXCL9 belongs to the CXC family of chemokines and participates in the regulation of leukocyte-trafficking and angiogenesis. Certain chemokines, including human MIG/CXCL9, exert strong antibacterial activity in vitro, although the importance of this property in vivo is unknown. In the present study, we investigated the expression and a possible role for MIG/CXCL9 in host defense during mucosal airway infection caused by Streptococcus pneumoniae in vivo. We found that intranasal challenge of C57BL/6 wild-type mice with pneumococci elicited production of high levels of MIG/CXCL9 in the lungs via the MyD88-dependent signaling pathway. Whereas both human and murine MIG/CXCL9 showed efficient killing of S. pneumoniae in vitro, MIG/CXCL9 knock-out mice were not more susceptible to pneumococcal infection. Our data demonstrate that, in vivo this chemokine probably has a redundant role, acting together with other antibacterial peptides and chemokines, in innate and adaptive host defense mechanisms against pneumococcal infections.
AuthorsMette Eliasson, Matthias Mörgelin, Joshua M Farber, Arne Egesten, Barbara Albiger
JournalMicrobes and infection / Institut Pasteur (Microbes Infect) Vol. 12 Issue 7 Pg. 565-73 (Jul 2010) ISSN: 1769-714X [Electronic] France
PMID20381636 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Anti-Infective Agents
  • CXC chemokine Mig
  • Chemokine CXCL9
  • Myeloid Differentiation Factor 88
  • Interferon-gamma
Topics
  • Animals
  • Anti-Infective Agents (metabolism)
  • Chemokine CXCL9 (metabolism)
  • Disease Models, Animal
  • Host-Pathogen Interactions
  • Humans
  • Interferon-gamma (pharmacology)
  • Lung (immunology, metabolism)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myeloid Differentiation Factor 88 (metabolism)
  • Pneumonia, Pneumococcal (immunology, metabolism)
  • Respiratory Mucosa (drug effects, immunology, metabolism)
  • Signal Transduction
  • Streptococcus pneumoniae (physiology)

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