Abstract

In pneumonia, bacteria induce changes in pulmonary surfactant. These changes are mediated by bacteria directly on secreted surfactant or indirectly through pulmonary type II epithelial cells. The bacterial component most likely responsible is endotoxin since gram-negative bacteria more often induce these changes than gram-positive bacteria. Also, endotoxin and gram-negative bacteria induce similar changes in surfactant. The interaction of bacteria or endotoxin with secreted surfactant results in changes in the physical (i.e. density and surface tension) properties of surfactant. In addition, gram-negative bacteria or endotoxin can injure type II epithelial cells causing them to produce abnormal quantities of surfactant, abnormal concentrations of phospholipids in surfactant, and abnormal compositions (i.e. type and saturation of fatty acids) of PC. The L/S ratio, the concentration of PG, and the amount of palmitic acid in PC are all significantly lower. The changes in surfactant have a deleterious effect on lung function characterized by significant decreases in total lung capacity, static compliance, diffusing capacity, and arterial PO2 and a significant increase in mean pulmonary arterial pressure. Also decreased concentrations of surfactant or an altered surfactant composition can result in the anatomic changes commonly seen in pneumonia such as pulmonary edema, hemorrhage, and atelectasis.

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