Inverse association between endogenous glucocorticoid secretion and L-selectin (CD62L) expression in trauma patients

Exogenously administered glucocorticoids downregulate inflammatory host res ponse, i.e. by inhibition of adhesion molecule expression on leukocyte surf aces. Here, possible associations between the trauma-induced endogenous sec retion of cortisol and the expression of neutrophil adhesion molecules (L- selectin/CD62L, CD11b, CD54) were studied in humans. Standardized elective hip arthroplasty was investigated as an exemplary condition of acute inflam mation. In 20 patients, blood for quantification of cortisol and adrenocort icotropic hormone was obtained at minutes 10, 20, 30, 60, hours 1, 2, 4 and 10 and days 1,3 and 7. Expression of L-selectin/CD62L, CD11b and CD54 on n eutrophil surfaces was determined preoperatively, and postoperatively at ho urs 1, 2, 3, 4, and 10 and at days 1 and 3. Secretion of both, adrenocortic otropic hormone and cortisol was significantly increased between 1-10 hours after onset of tissue injury. Compared to baseline values, CD11b expressio n was increased at hour 1 and normalized after day 1, whereas L-selectin/CD 62L expression, mirroring this pattern was decreased until day 1. Patients with high endogenous glucocorticoid secretion exhibited significantly decre ased expression selectively of L-selectin/CD62L. However, we also observed that glucocorticoids do not directly induce L-selectin shedding from neutro phil surfaces in vitro, arguing for more indirect glucocorticoid action on adhesion molecule expression. Together, this study showed that increased en dogenous cortisol secretion is associated with lower expression of L-select in on neutrophil surfaces in humans that is consistent with a downmodulatin g role of this neuroendocrine stress response in inflammatory leukocyte rec ruitment.