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Chlamydia pneumoniae facilitates monocyte adhesion to endothelial and smooth muscle cells
1Section of Infectious Diseases, Department of Pediatrics, University of California Davis, CA 95616, USA. rkkaul@ucdavis.edu
Insights
Chlamydia pneumoniae can infect human monocytes, enabling them to adhere to artery cells. This suggests a mechanism for how Chlamydia pneumoniae contributes to atherosclerosis development.
Area of Science:
- Infectious diseases
- Cardiovascular research
- Cell biology
Background:
- Chlamydia pneumoniae infection is associated with atherosclerotic heart disease.
- The mechanism by which C. pneumoniae accesses atheromatous lesions remains unclear.
- Infected circulatory components adhering to vascular cells may initiate inflammation.
Purpose of the Study:
- To investigate the susceptibility of human monocytes to C. pneumoniae infection.
- To determine if C. pneumoniae-infected monocytes adhere to human coronary artery endothelial cells (HCAEC) and smooth muscle cells (HCSMC).
Main Methods:
- Human monocytes were infected in vitro with viable or heat-inactivated C. pneumoniae.
- Infection was confirmed by observing chlamydial inclusions.
- Adherence of infected and uninfected monocytes to HCAEC and HCSMC was quantified.
Main Results:
- Monocytes were successfully infected by viable C. pneumoniae, showing characteristic inclusions.
- Heat-inactivated C. pneumoniae did not infect monocytes, with no inclusions observed.
- Monocytes infected with viable C. pneumoniae exhibited significantly increased adherence to HCAEC and HCSMC.
Conclusions:
- Human monocytes are susceptible to C. pneumoniae infection in vitro.
- C. pneumoniae infection enhances monocyte adherence to coronary artery cells.
- This enhanced adherence may represent a key step in C. pneumoniae's role in atherosclerosis pathogenesis.
Abstract:
Chlamydia pneumoniae has been linked to atherosclerotic heart disease. However, there is a limited knowledge by which C. pneumoniae gain access to atheromatous lesions. The adhesion of C. pneumoniae -infected circulatory component(s) to endothelium and smooth muscle cells represents the first step in an inflammatory response. We examined the ability of viable as well as heat inactivated C. pneumoniae to infect human monocytes and subsequently the ability of infected monocytes to adhere to human coronary artery endothelial cells (HCAEC) and human coronary smooth muscle cells (HCSMC). Our results demonstrate susceptibility of monocytes to in vitro chlamydial infection. Inclusions of varying sizes and intensities were observed 3-5 days after inoculation with viable C. pneumoniae. Monocytes infected with heat inactivated organisms revealed no inclusions, in keeping with the observations of uninfected monocytes. Moreover, monocytes infected with viable C. pneumoniae adhered preferentially to HCAEC and HCSMC, as compared to uninfected monocytes or monocytes harbouring heat inactivated Chlamydia.