Elevation in pulmonary neutrophils and prolonged production of pulmonary macrophage inflammatory protein-2 after burn injury with prior alcohol exposure.
Various studies have shown that alcohol exposure before thermal injury leads to increased morbidity and mortality. Pulmonary failure is a major complication seen in these patients. This study examines the effects of prior alcohol exposure on lung pathology after burn injury. There is a marked increase in neutrophil recruitment in the lung after thermal injury, and herein we show that this appears to be significantly elevated in animals given alcohol before burn injury. Consequently, we chose to determine whether there is a difference in pulmonary production of macrophage inflammatory protein (MIP)-2, a potent neutrophil chemoattractant, in mice subjected to a 15% total body surface area scald (or sham) injury with or without prior ethanol treatment. Lung tissue was obtained at various time points after injury and homogenates were assayed for MIP-2 by enzyme-linked immunosorbent assay. At 2 h after injury, peak levels of the chemokine were produced in both burn and burn + alcohol-treated mice. This represents a 7-fold increase above baseline. In mice exposed to burn injury alone, the level of MIP-2 returned to baseline within 8 h. In contrast, mice given alcohol before burn injury continued to show elevated levels of the chemokine at 8 h, after which MIP-2 decreased. This study may provide a basis for understanding the mechanism responsible for the increased neutrophil presence in the lung after thermal injury in individuals who have consumed alcohol. Subsequently, this may lead to the enhanced neutrophil-mediated pulmonary damage observed in these patients.
Patel
P J
PJ
Department of Cell Biology, Neurobiology, and Anatomy, Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Faunce
D E
DE
Gregory
M S
MS
Duffner
L A
LA
Kovacs
E J
EJ
D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D002056:Burns / Q000378:metabolism*; D054426:Chemokine CXCL2; D008168:Lung / Q000033:anatomy & histology / Q000378:metabolism*; D008297:Male; D051379:Mice; D015846:Monokines / Q000032:analysis / Q000096:biosynthesis*; D009504:Neutrophils / Q000378:metabolism*; D012774:Shock, Traumatic / Q000378:metabolism*; D013997:Time Factors
D054426:Chemokine CXCL2; D015846:Monokines