We have previously shown that endotoxin reduces pulmonary inflammation associated with O2 toxicity in the rat and causes loss of L-selectin from the neutrophil surface. We measured the expression of the adhesion molecules, E-selectin and ICAM-1, using immunostaining of rat lung frozen sections and soluble (s) L-selectin from rat serum using an ELISA after 2,6,24,30,48 and 60 hours of in vivo O2 exposure. The degree of staining for E-selectin was scored as 0-4; mean ± S.D. For sL-selectin, data are presented as absorbance minus IgG control (Air =.095±.021). ICAM-1 expression in lung tissue was high and did not differ with LPS or O2. We conclude that 1) E-selectin in O2 controls is markedly higher after 60 hrs of hyperoxia; 2) E-selectin rises acutely after LPS and is higher than O2 controls at 6 and 24 hours. However, it declines and is significantly lower than O2 control levels after 60 hrs; and 3) soluble L-selectin declines after LPS, but is back to O2 control levels by 48-60 hrs. We speculate that the pattern of low soluble L-selectin early after LPS may reflect the upregulation of a ligand for L-selectin in pulmonary tissue. The lower expression of E-selectin after 60 hrs of O2 in LPS-treated rats may contribute to decreased pulmonary inflammation after hyperoxia. Table
