Efectos in vitro de la infección por Chlamydia pneumoniae en células implicadas en el proceso aterogénico

Laburpena

Background Experimental studies indicate the possible pathogenic effects of vascular wall infections and recognize that they play a role in the various phenomena accompanying the formation of atheromatous plaque. Objective To evaluate the morphodynamic characteristics of different types of normalhumancells of the vascular wall before and after infection with Chlamydia pneumoniae (CP). Material and methods Cultures of human epithelial cells, monocytes and lymphocytes from peripheral blood, endothelial cells, fibroblasts and smooth muscle cells were inoculated with a standardized CP strain. The techniques of video intervalometry and phase contrast digital microscopy were used to evaluate the morphodynamic characteristics of the cells and immunofluorescence was used to detect CP. Results In epithelial cells, CP infection provoked two types of degeneration: early (at 8 hours) and rapid (lasting 1-2 hours). The other type of cellular degeneration occurred later (at 16 hours) and was slower (lasting approximately 20 hours). Mitotic activity decreased in the first few days, recovering after 5-6 days and returning to normal on the ninth day. In monocyte cultures, CP provoked a type of cellular degeneration withvacuolization (vacuoles with inclusion bodies).The maximum rate of degeneration was obtainedafter 1 week, except in lymphocytes, where degeneration was more rapid. Endothelial cells infected with CP formed aggregates when they died, showing rapid first kinetics and slow second kinetics. Mitotic activity decreased and then increased a few days later. Fibroblasts showed a high rate (nearly 20%) of degeneration. Degenerated cells did not form aggregates. Smooth muscle cells transformed into foam cells under the influence of CP infection. Conclusions The finding that all the cells were susceptible to degeneration and transformation indicates that infection may initiate a phenomenon of endothelial dysfunction, maintaining the chronic inflammatory component in the wall, and provoking instability of atheromatous plaques.