Trauma alters alveolar effector cell apoptosis

The lung's immune response to trauma is biphasic with an initial proinflammatory and a subsequent anti-inflammatory cytokine response that alters cell function. Apoptosis, programmed cell death, is regulated by cytokines, and alteration of this important cellular function has been associated with end-organ dysfunction. We hypothesize that the lung's immune response to trauma alters alveolar inflammatory cell apoptosis and may contribute to posttrauma pulmonary dysfunction.

Bronchoalveolar lavage specimens were obtained from trauma patients with an injury severity score of 16 or more compared with patients who underwent elective surgery. Interleukin (IL)-8 and IL-10 were measured in the supernatant. Apoptosis and HLA-DR expression were measured in the cellular content, and Pao(2)/Fio(2) ratios were calculated as a measure of pulmonary function.

After trauma, the alveolar inflammatory cell population was composed primarily of neutrophils. Apoptosis was suppressed initially after injury but increased to control levels by 72 hours after injury in parallel to alveolar concentrations of IL-10. Levels of IL-8 remained elevated, and HLA-DR expression remained suppressed throughout the study period. Pao(2)/Fio(2) ratios demonstrated pulmonary dysfunction by 72 hours.

The lung's biphasic cytokine response to injury significantly alters both alveolar inflammatory cell apoptosis and HLA-DR expression. The alteration of alveolar inflammatory cell apoptosis may be dependent on the local production of IL-10. A reduction in apoptosis immediately preceded the onset of clinically significant pulmonary dysfunction.