Consequences of Hypoxia for the Pulmonary Alveolar Epithelial Cell Innate Immune Response.

Pulmonary innate immune responses involve a highly regulated multicellular network to defend the enormous surface area of the lung. Disruption of these responses renders the host susceptible to pneumonia. Alveolar epithelial cells (AEC) are a critical source of innate immune molecules such as GM-CSF, which determine the functional maturation of alveolar macrophages.

Mechanisms of suppression of alveolar epithelial cell GM-CSF expression in the setting of hyperoxic stress.

Pulmonary expression of granulocyte/macrophage colony-stimulating factor (GM-CSF) is critically important for normal functional maturation of alveolar macrophages. We found previously that lung GM-CSF is dramatically suppressed in mice exposed to hyperoxia. Alveolar epithelial cells (AEC) are a major source of GM-CSF in the peripheral lung, and in vivo hyperoxia resulted in greatly reduced expression of GM-CSF protein by AEC ex vivo.

Community-acquired pneumonia in adults.

The most common etiologic agent of CAP is Streptococcus pneumoniae. Atypical pathogens are the cause in approximately 20% to 30% of patients. Because the patients clinical presentation cannot be used to predict if a patient is infected with S.