title: Restraint stress-induced elevation of endogenous glucocorticoid suppresses migration of granulocytes and macrophages to an inflammatory locus.
abstract: It has been reported that restraint stress gives rise to various immunosuppressive events. In the present study, we focused our interest on an early stage of the host-defense system in which granulocytes, macrophages and natural killer (NK) cells are involved. We observed that an elevation of endogenous glucocorticoid levels in mice induced by 24 h-restraint stress (acute stress) did not significantly reduce the NK activity of the spleen cells but profoundly suppressed the migration of macrophages and granulocytes into peritoneal cavities of the mice at 24 h after an intraperitoneal injection of proteose peptone. The reduced number of the migrated granulocytes and macrophages corresponded to a down-regulated gene expression of such chemotactic factors as MCP-1/JE in the peritoneal exudate cells of the stress-loaded mice. The stress-loaded mice recovered from such a suppressive state upon treatment with the glucocorticoid antagonist, RU-486, or upon adrenalectomy, suggesting that the elevated level of endogenous glucocorticoid is responsible for these suppressive effects of acute stress.
authors.affiliation: Department of Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi-Ku, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Mizobe
authors.forename: K
authors.initials: K
authors.lastname: Kishihara
authors.forename: R
authors.initials: R
authors.lastname: Ezz-Din El-Naggar
authors.forename: G A
authors.initials: GA
authors.lastname: Madkour
authors.forename: C
authors.initials: C
authors.lastname: Kubo
authors.forename: K
authors.initials: K
authors.lastname: Nomoto
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D001202:Ascitic Fluid / Q000473:pathology; D001483:Base Sequence; D002452:Cell Count / Q000187:drug effects; D002465:Cell Movement; D018932:Chemokine CCL2 / Q000235:genetics; D003345:Corticosterone / Q000097:blood*; D003907:Dexamethasone / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D006098:Granulocytes / Q000502:physiology*; D007694:Killer Cells, Natural / Q000502:physiology; D008264:Macrophages / Q000502:physiology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D015735:Mifepristone / Q000494:pharmacology; D008969:Molecular Sequence Data; D010538:Peritonitis / Q000097:blood* / Q000473:pathology* / Q000503:physiopathology; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000097:blood*; D013950:Thymus Gland / Q000473:pathology
chemical_list: D018932:Chemokine CCL2; D015735:Mifepristone; D003907:Dexamethasone; D003345:Corticosterone