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 pat ients 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 m easured in bronchoalveolar lavage (BAL)fluid from multitrauma patients on a dmission, 24, 48, and 72 hours post-injury and following lipopolysaccharide (LPS) induction of alveolar cells. Patients were compared based on IL-8 le vels and the development of AT. Results. A high level of IL-8 on admission was associated with the, develop ment of NP In addition, levels of IL-8 were significantly greater in AT-pos itive patients at all time points. The IL-10 levels decreased from admissio n values in AT-negative patients but increased in AT-positive patients. Fur thermore, 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 patie nts 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 a nd severe IL-8 process within the lung followed by an exaggerated IL-10 res ponse that may inhibit effector cell function.