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Interaction of Chlamydia pneumoniae and human alveolar macrophages: infection and inflammatory response
V Redecke1, K Dalhoff, S Bohnet
1Department of Medicine II and Institute of Medical Microbiology, Medical University of Lübeck, Lübeck, Germany.
Abstract:
The obligate intracellular pathogen Chlamydia pneumoniae is associated with chronic respiratory, atherosclerotic, and rheumatic disease. The alveolar macrophage (AM) is a potential target cell for the pathogen and may contribute to respiratory immunopathology. We therefore investigated in vitro the interaction between chlamydiae and macrophages with cocultures of C. pneumoniae and AM from 12 healthy volunteers. Inflammatory responses were evaluated through lucigenin-amplified chemiluminescence; secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin 8 (IL-8); and expression of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen-DR (HLA-DR). C. pneumoniae readily induced productive infection in the AM. Inclusions containing replicating pathogens could be maintained for up to 120 h. Morphologically similar infection patterns were seen ex vivo in AM collected from six patients with known C. pneumoniae pneumonia. AM responded to the infection with a marked, dose-dependent release of reactive oxygen species, TNF-alpha, IL-1beta, and IL-8. ICAM-1 expression remained unchanged, but HLA-DR was significantly upregulated. Our data indicate that the release of antimicrobial mediators cannot prevent chlamydial infection and replication in AM, but may be involved in amplification of the local inflammatory response in C. pneumoniae pneumonia.
Insights
Chlamydia pneumoniae infects alveolar macrophages, triggering inflammatory responses like reactive oxygen species and cytokine release. However, these responses do not prevent pathogen replication, potentially amplifying C. pneumoniae pneumonia.
Area of Science:
- Immunology
- Microbiology
- Pathogen-Host Interactions
Background:
- Chlamydia pneumoniae is an obligate intracellular pathogen linked to chronic respiratory, atherosclerotic, and rheumatic diseases.
- Alveolar macrophages (AMs) are key immune cells in the lungs and a potential target for C. pneumoniae, possibly contributing to respiratory immunopathology.
Purpose of the Study:
- To investigate the in vitro interaction between C. pneumoniae and AMs.
- To evaluate the inflammatory responses of AMs upon infection with C. pneumoniae.
Main Methods:
- Cocultures of C. pneumoniae and AMs from healthy volunteers were used.
- Inflammatory responses were assessed via chemiluminescence, cytokine secretion (TNF-alpha, IL-1beta, IL-8), and cell surface molecule expression (ICAM-1, HLA-DR).
- Ex vivo AMs from C. pneumoniae pneumonia patients were also examined.
Main Results:
- C. pneumoniae established productive infections in AMs, with replicating pathogens observed for up to 120 hours.
- Infected AMs released reactive oxygen species, TNF-alpha, IL-1beta, and IL-8 in a dose-dependent manner.
- HLA-DR expression was significantly upregulated, while ICAM-1 remained unchanged.
Conclusions:
- Antimicrobial mediator release by AMs does not inhibit C. pneumoniae infection and replication.
- AM inflammatory responses may amplify the local inflammatory process in C. pneumoniae pneumonia.
- Alveolar macrophages are susceptible to C. pneumoniae infection and contribute to the host's inflammatory response.