Role of host cell metabolism in the pathogenesis of Mycoplasma pneumoniae infection

Publisher Website
Google Scholar
Abstract
Human lung fibrolasts develop a cytopathic effect (CPE) when infected with M. pneumoniae. The relationship between host cell metabolism and the formation of the CPE was studied. Human lung fibroblasts were grown in different serum concentrations, plated at different densities, and grown for different periods of time to alter the metabolic activity of the cells. DNA, RNA and protein syntheses were measured by the ability of the cells to incorporate thymidine, uridine and leucine, respecitvely. With each treatment, leucine incorporation remained constant. Thymidine and uridine incorporation was higher when the cells were in high serum, at low cell densities or grown for 2 or 3 days. The appearance of an observable CPE, which was corroborated with a protein synthesis assay, correlated closely with thymidine and uridine incorporation. A more pronounced CPE was seen when thymidine and uridine incorporation was high. The first 2 h after infection by M. pneumoniae were the critical hours in determining whether a CPE would develop. This was accomplished by altering the serum concentration of the culture medium at different times postinfection and thereby altering the metabolism of the fibroblasts. The importance of the metabolic state of the host cells in studying mycoplasma infections was demonstrated and a correlation between the nucleic acid metabolism of the cells and the production of a CPE was established.