Trauma alters alveolar effector cell apoptosis.
BACKGROUND
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Hoth
J Jason
JJ
Department of Surgery, University of Louisville, Louisville, KY 40292, USA.
Scott
Melanie J
MJ
Owens
Roger K
RK
Stassen
Nicole A
NA
Franklin
Glen A
GA
Cheadle
William G
WG
Rodriguez
Jorge L
JL
D000328:Adult; D017209:Apoptosis; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology; D016753:Interleukin-10 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D055370:Lung Injury; D008297:Male; D009504:Neutrophils / Q000473:pathology; D010100:Oxygen / Q000097:blood; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011651:Pulmonary Artery; D012119:Respiration; D013997:Time Factors; D015599:Trauma Severity Indices; D014947:Wounds and Injuries / Q000503:physiopathology
D006684:HLA-DR Antigens; D016209:Interleukin-8; D016753:Interleukin-10; D010100:Oxygen