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Background   Chlamydia pneumoniae  is a common human pathogen that is associated with upper and lower respiratory tract infections. It has also been suggested that  C. pneumoniae  infection can trigger or promote a number of chronic inflammatory conditions, including asthma and atherosclerosis. Several strains of  C. pneumoniae  have been isolated from humans and animals, and sequence data demonstrates marked genetic conservation, leaving unanswered the question as to why chronic inflammatory conditions may occur following some respiratory-acquired infections.    Methods   C. pneumoniae  strains AR39 and AO3 were used  in vitro  to infect murine bone marrow derived macrophages and L929 fibroblasts, or  in vivo  to infect C57BL/6 mice via the intranasal route.    Results  We undertook a comparative study of a respiratory isolate, AR39, and an atheroma isolate, AO3, to determine if bacterial growth and host responses to infection varied between these two strains. We observed differential growth depending on the host cell type and the growth temperature; however both strains were capable of forming plaques  in vitro . The host response to the respiratory isolate was found to be more inflammatory both  in vitro , in terms of inflammatory cytokine induction, and  in vivo , as measured by clinical response and lung inflammatory markers using a mouse model of respiratory infection.    Conclusions  Our data demonstrates that a subset of  C. pneumoniae  strains is capable of evading host innate immune defenses during the acute respiratory infection. Further studies on the genetic basis for these differences on both the host and pathogen side could enhance our understanding how  C. pneumoniae  contributes to the development chronic inflammation at local and distant sites.

bmc microbiology

Comparative analysis of the growth and biological activity of a respiratory and atheroma isolate of Chlamydia pneumoniae reveals strain-dependent differences in inflammatory activity and innate immune evasion