Cytokines and the pathogenesis of nosocomial pneumonia

Background. Nosocomial pneumonia (AT) in injured patients is a significant clinical problem. Me hypothesize that the pathogenesis of NP in injured patients involves an imbalanced cytokine response within the alveolar airspace that may inhibit effector cell function. Methods. Proinflammatory (IL-8) and anti-inflammatory (IL-10) levels were measured in bronchoalveolar lavage (BAL)fluid from multitrauma patients on admission, 24, 48, and 72 hours post-injury and following lipopolysaccharide (LPS) induction of alveolar cells. Patients were compared based on IL-8 levels and the development of AT. Results. A high level of IL-8 on admission was associated with the, development of NP In addition, levels of IL-8 were significantly greater in AT-positive patients at all time points. The IL-10 levels decreased from admission values in AT-negative patients but increased in AT-positive patients. Furthermore, a high level of IL-10 ( > 120 pg/mL) at 72 hours post-injury was associated With the development of AT Alveolar cells from AT-positive patients produced significantly more IL-10 in response to LPS than cells from AT-negative patients. Conclusions. The pathogenesis of AT in injured patients involves an early and severe IL-8 process within the lung followed by an exaggerated IL-10 response that may inhibit effector cell function.