부산대학교 도서관

Byline: Susan E. Keeney (1), Mary J. Mathews (1), Karen E. Shattuck (1), Dara V. Dallas (1) Keywords: lung; selectins; L-selectin; lipopolysaccharide; adhesion molecules Abstract: The mechanisms by which sublethal doses of endotoxin protect against hyperoxic lung injury are not completely understood. We hypothesized that endotoxin treatment would result in a decreased inflammatory response to hyperoxia and that this would be accompanied by activation of neutrophils (as evidenced by loss of L-selectin) in the peripheral circulation. Adult rats were injected with endotoxin 0.5 mg/kg prior to and 24 hr after onset of exposure to aY=98% O.sub.2. After 56 hr of hyperoxia, pulmonary neutrophils were lower in the O.sub.2/endotoxin group compared to O.sub.2 controls as measured by myeloperoxidase in lung homogenates and neutrophil counts in bronchoalveolar lavage fluid. Circulating neutrophils were also significantly lower in the O.sub.2/endotoxin group compared to O.sub.2 controls at 56 hr. Expression of the neutrophil adhesion molecule, L-selectin, was lower at 4 and 24 hr in the endotoxin-treated rats compared to O.sub.2 controls. There were no differences at 48 hr. Expression of CD18 rose significantly in the O.sub.2/endotoxin group after 4 hr, but thereafter did not differ from O.sub.2 controls. In summary, endotoxin protection from O.sub.2 toxicity was associated with reduced neutrophils in the lung and a loss of L-selectin from peripheral blood neutrophils. Author Affiliation: (1) Department of Pediatrics, University of Texas Medical Branch, Galveston, TX, 77555 Article History: Registration Date: 12/10/2004