Regulation of Proinflammatory Cytokines in Human Lung Epithelial Cells Infected withMycoplasma pneumoniae

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Abstract
Mycoplasma pneumoniaeis a small bacterium without a cell wall that causes tracheobronchitis and atypical pneumonia in humans. It has also been associated with chronic conditions, such as arthritis, and extrapulmonary complications, such as encephalitis. Although the interaction of mycoplasmas with respiratory epithelial cells is a critical early phase of pathogenesis, little is known about the cascade of events initiated by infection of respiratory epithelial cells by mycoplasmas. Previous studies have shown thatM. pneumoniaecan induce proinflammatory cytokines in several different study systems including cultured murine and human monocytes. In this study, we demonstrate thatM. pneumoniaeinfection also induces proinflammatory cytokine expression in A549 human lung carcinoma cells. Infection of A549 cells resulted in increased levels of interleukin-8 (IL-8) and tumor necrosis factor alpha mRNA, and both proteins were secreted into culture medium. IL-1β mRNA also increased after infection and IL-1β protein was synthesized, but it remained intracellular. In contrast, levels of IL-6 and gamma interferon mRNA and protein remained unchanged or undetectable. Using protease digestion and antibody blocking methods, we found thatM. pneumoniaecytadherence is important for the induction of cytokines. On the other hand, whileM. pneumoniaeprotein synthesis and DNA synthesis do not appear to be prerequisites for the induction of cytokine gene expression, A549 cellular de novo protein synthesis is responsible for the increased cytokine protein levels. These results suggest a novel role for lung epithelial cells in the pathogenesis ofM. pneumoniaeinfection and provide a better understanding ofM. pneumoniaepathology at the cellular level.