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1 Institute for Medical Microbiology and Hygiene, 2 Institute for Pathology, University of Lübeck, Lübeck and 3 Research Center Borstel, Division of Molecular Infection Biology, Borstel, Germany
CORRESPONDENCE: J. Gieffers, Institute for Medical Microbiology and Hygiene, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. Fax: 49 4515002808. E-mail: jens.gieffers@hygiene.ukl.mu-luebeck.de
Keywords: animal model, chlamydia, dissemination, macrophages, monocytes, vascular infection
Received: August 13, 2003
Accepted November 25, 2003
This study was supported by a grant from the Deutsche Forschungsgemeinschaft to M. Maass (SFB 367, B11).
Abstract
Chlamydia pneumoniae, a major cause of community-acquired pneumonia, primarily infects the respiratory tract. Chronic infection of nonrespiratory sites, such as the vascular wall, the brain or blood monocytes, requires evasion from the lungs and spreading via the bloodstream. The cell types involved in dissemination are insufficiently characterised.
In this study, New Zealand White rabbits were infected intratracheally with C. pneumoniae, and lung manifestation and systemic dissemination were monitored by polymerase chain reaction and immunohistochemistry. Infection of the lungs was characterised by an early phase dominated by granulocytes and a late phase dominated by alveolar macrophages (AM).
Granulocytes, AM and alveolar epithelial cells acted as host cells for chlamydiae, which remained detectable for up to 8 weeks. AM transported the pathogen to the peribronchiolar lymphatic tissue, and subsequently C. pneumoniae entered the spleen and the aorta via dissemination by peripheral blood monocytes.
In conclusion, Chlamydia pneumoniae-infected alveolar macrophages transmigrate through the mucosal barrier, and give the pathogen access to the lymphatic system and the systemic circulation. Infected peripheral blood monocytes are the vector system within the bloodstream and transmit the infection to the vascular wall. This is the first description of granulocytes acting as a reservoir for Chlamydia pneumoniae early in infection.
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