PAF Receptor Anchors Streptococcus Pneumoniae to Activated Human Endothelial Cells

Abstract

Streptococcus pneumoniae is a Gram positive bacteria that is a major cause of pneumonia, sepsis, and meningitis¹. In contrast to the severity of invasive disease, ~40% of individuals harbor pneumococcus asymptomatically in the nasopharynx². Further, it has long been recognized that the mere presence of pneumococci in the pulmonary alveolus does not infer progression to pneumonia^3,4. These disparate courses suggest that as yet unknown elements of the encounter between host and pathogen determine the outcome. A clinical clue to the nature of these elements is the observation of the propensity of patients and experimental animals to progress to bacterial pneumonia in the context of an intercurrent upper respiratory tract viral infection⁵. Taken together with the recent observation that pneumococci have been shown to adhere in greater numbers to virally infected cells in vitro⁶, we hypothesized a change from a state of simple bacterial binding to the surface of the nasopharyngeal or pulmonary epithelium to a state promoting translocation across underlying endothelial cells into the blood stream in the context of an inflammatory stimulus.