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Monocyte-endothelial cell coculture enhances infection of endothelial cells with Chlamydia pneumoniae
T M Lin1, L A Campbell, M E Rosenfeld
1National Cheng Kung University, College of Medicine, Department of Medical Technology, Tainan, Taiwan.
Abstract:
To determine the mechanism(s) by which Chlamydia pneumoniae homes to and establishes persistent infection in atheromatous lesions, the effect of the interaction of monocytes/macrophages (U937 cells) with human umbilical vein endothelial cells (HUVECs) and transformed human arterial endothelial cells (HMEC-1s) on the susceptibility of endothelial cells to infection with C. pneumoniae was investigated. Infection was enhanced 4.7-fold (HUVECs) and 4.4-fold (HMEC-1s) after coculture at monocyte-to-endothelial cell ratios of 5 and 2.5, respectively. U937 cells also directly transmitted infection to the endothelial cells, and addition of U937 cell-conditioned media dose-dependently enhanced the infectivity 2.0- to 2.5-fold. The stimulation of infectivity was specific to endothelial cells, because coculturing of monocytes with epithelial cells did not enhance the susceptibility of epithelial cells to infection. The susceptibility of endothelial cells to infection with C. trachomatis and C. psittaci was not enhanced by the monocyte-derived factor(s).
Insights
Monocyte-macrophages enhance Chlamydia pneumoniae infection in endothelial cells, contributing to persistent infection in atherosclerosis. This interaction specifically targets arterial cells, not epithelial cells.
Area of Science:
- Microbiology
- Immunology
- Cardiovascular Research
Background:
- Chlamydia pneumoniae is implicated in atherosclerosis.
- The mechanisms of C. pneumoniae persistence in atheromatous lesions are not fully understood.
- Monocyte-macrophage interactions with endothelial cells may influence infection dynamics.
Purpose of the Study:
- To investigate how monocyte/macrophage interaction with endothelial cells affects susceptibility to Chlamydia pneumoniae infection.
- To elucidate the role of monocytes/macrophages in the establishment of persistent C. pneumoniae infection in atheromatous lesions.
Main Methods:
- Coculturing U937 monocyte/macrophage cells with human umbilical vein endothelial cells (HUVECs) and human microvascular endothelial cells (HMEC-1s).
- Assessing endothelial cell susceptibility to C. pneumoniae infection after coculture.
- Evaluating the effect of U937 cell-conditioned media on endothelial cell infectivity.
- Comparing infection enhancement in endothelial cells versus epithelial cells.
Main Results:
- Coculture significantly enhanced C. pneumoniae infection in HUVECs (4.7-fold) and HMEC-1s (4.4-fold).
- U937 cells directly transmitted infection and U937-conditioned media dose-dependently increased infectivity (2.0- to 2.5-fold).
- Enhanced susceptibility was specific to endothelial cells; epithelial cells showed no increased infection.
Conclusions:
- Monocyte-macrophage interactions significantly increase endothelial cell susceptibility to Chlamydia pneumoniae.
- This interaction may be a key mechanism for C. pneumoniae homing and establishing persistent infections in atheromatous lesions.
- The enhancing factor(s) appear specific to endothelial cells and do not affect other cell types or Chlamydia species.