title: Inverse association between endogenous glucocorticoid secretion and L-selectin (CD62L) expression in trauma patients.
abstract: Exogenously administered glucocorticoids downregulate inflammatory host response, i.e. by inhibition of adhesion molecule expression on leukocyte surfaces. Here, possible associations between the trauma-induced endogenous secretion of cortisol and the expression of neutrophil adhesion molecules (L-selectin/CD62L, CD 11b, CD54) were studied in humans. Standardized elective hip arthroplasty was investigated as an exemplary condition of acute inflammation. In 20 patients, blood for quantification of cortisol and adrenocorticotropic 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 neutrophil surfaces was determined preoperatively, and postoperatively at hours 1, 2, 3, 4, and 10 and at days 1 and 3. Secretion of both, adrenocorticotropic hormone and cortisol was significantly increased between 1-10 hours after onset of tissue injury. Compared to baseline values, CD11b expression was increased at hour 1 and normalized after day 1, whereas L-selectin/CD62L expression, mirroring this pattern was decreased until day 1. Patients with high endogenous glucocorticoid secretion exhibited significantly decreased expression selectively of L-selectin/CD62L. However, we also observed that glucocorticoids do not directly induce L-selectin shedding from neutrophil surfaces in vitro, arguing for more indirect glucocorticoid action on adhesion molecule expression. Together, this study showed that increased endogenous cortisol secretion is associated with lower expression of L-selectin on neutrophil surfaces in humans that is consistent with a downmodulating role of this neuroendocrine stress response in inflammatory leukocyte recruitment.
authors.affiliation: Department of Neurology, University of Heidelberg, Mannheim, FRG.
authors.forename: K
authors.initials: K
authors.lastname: Fassbender
authors.forename: S
authors.initials: S
authors.lastname: Kaptur
authors.forename: P
authors.initials: P
authors.lastname: Becker
authors.forename: J
authors.initials: J
authors.lastname: Gröschel
authors.forename: R
authors.initials: R
authors.lastname: Schmidt
authors.forename: M
authors.initials: M
authors.lastname: Hennerici
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000368:Aged; D019644:Arthroplasty, Replacement, Hip; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D019041:L-Selectin / Q000096:biosynthesis*; D007958:Leukocyte Count; D008137:Longitudinal Studies; D016177:Macrophage-1 Antigen / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D020556:Neutrophil Infiltration / Q000502:physiology; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000502:physiology*; D015207:Osteoarthritis, Hip / Q000097:blood / Q000473:pathology / Q000601:surgery; D010913:Pituitary-Adrenal System / Q000502:physiology
chemical_list: D016177:Macrophage-1 Antigen; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone