title: Contribution of plasma cortisol to corticosteroid-suppressed peripheral blood natural killer cell activity in Crohn's disease.
abstract: We recently showed that patients with active ileocecal Crohn's disease (CD) have a temporarily suppressed peripheral blood natural killer (NK) cell activity during treatment with oral budesonide or prednisolone. This suppression was caused by a decrease in the number of CD16+ NK cells in the circulation. In the present study we evaluated the contribution of cortisol in plasma to this suppressed NK cell activity. The CD patients took part in a controlled study where they received either oral budesonide or prednisolone for 10 weeks. Before treatment, and at 4 and 10 weeks of treatment, peripheral blood NK cell activity, numbers of circulating CD16+ NK cells, and plasma cortisol levels were analysed. These parameters were determined both before and 30 min after administration of adrenocorticotropic hormone (ACTH). The ACTH-induced plasma cortisol increase was accompanied by a stimulated NK cell activity, when both are suppressed by corticosteroid treatment, without changing the number of CD16+ NK cells. Therefore, a low plasma cortisol level contributes to the corticosteroid mediated NK cell suppression in active ileocecal CD.
authors.affiliation: Department of Gastroenterology and Hepatology, University Hospital Leiden, Netherlands.
authors.forename: G J
authors.initials: GJ
authors.lastname: van Ierssel
authors.forename: A
authors.initials: A
authors.lastname: van der Sluys Veer
authors.forename: H W
authors.initials: HW
authors.lastname: Verspaget
authors.forename: G
authors.initials: G
authors.lastname: Griffioen
authors.forename: R A
authors.initials: RA
authors.lastname: van Hogezand
authors.forename: C B
authors.initials: CB
authors.lastname: Lamers
mesh_terms: D000284:Administration, Oral; D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage / Q000494:pharmacology; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D019819:Budesonide; D003424:Crohn Disease / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D007694:Killer Cells, Natural / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D018655:Lymphocyte Count / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000008:administration & dosage / Q000627:therapeutic use; D011282:Pregnenediones / Q000008:administration & dosage / Q000627:therapeutic use; D017452:Receptors, IgG / Q000187:drug effects / Q000235:genetics
chemical_list: D000893:Anti-Inflammatory Agents; D011282:Pregnenediones; D017452:Receptors, IgG; D019819:Budesonide; D000324:Adrenocorticotropic Hormone; D011239:Prednisolone; D006854:Hydrocortisone