Ectopic lymphoid tissue formation in the lungs of mice infected with Chlamydia pneumoniae is associated with epithelial macrophage inflammatory protein-2/CXCL2 expression

P. M. Fitch, N. M. Wheelhouse, P. Bowles, M. Paterson, D. Longbottom, Gary Entrican, S. E. M. Howie

Research output: Contribution to journalArticlepeer-review

Abstract

Infection with Chlamydia pneumoniae (Cp) accounts for around 10% of community acquired bacterial pneumonia and has been associated with other chronic inflammatory conditions. We describe a C57/Bl6 murine model of Cp lung infection characterized by a dose-dependent, resolving neutrophilia followed by lymphocytic infiltration of the lungs. By 21 days post-infection, mice exhibit a T helper type 1 (Th1) polarized serum antibody response with local mucosal antibody secretion and organization of ectopic lymphoid tissue which persisted in the absence of detectable Cp DNA. Macrophage inflammatory protein (MIP)-2/CXCL2, which recruits neutrophils and lymphocytes and is associated with ectopic lymphoid tissue formation, was secreted in the lungs post-infection. In vitro, lung epithelial cells up-regulated MIP-2/CXCL2 in response to both rough lipopolysaccharide (reLPS) and Cp infection. We conclude that Cp infection can have long-term inflammatory effects on tissue that persist after clearance of active infection.

Original languageEnglish
Pages (from-to)372-378
Number of pages7
JournalClinical & Experimental Immunology
Volume162
Issue number2
DOIs
Publication statusPublished - Nov 2010

Keywords

  • Chlamydia pneumoniae
  • CXCL2/MIP-2
  • epithelium
  • lung
  • lymphocytes

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