title: Age-related bias in function of natural killer T cells and granulocytes after stress: reciprocal association of steroid hormones and sympathetic nerves.
abstract: Stress-associated immune responses were compared between young (8 weeks of age) and old (56 weeks) mice. Since stress suppresses the conventional immune system (i.e. T and B cells) but inversely activates the primordial immune system (i.e. extrathymic T cells, NKT cells, and granulocytes), these parameters were analysed after restraint stress for 24 h. The thymus became atrophic as a function of age, and an age-related increase in the number of lymphocytes was seen in the liver. Although the number of lymphocytes in both the thymus and liver decreased as the result of stress, the magnitude was much more prominent in the thymus. To determine stress-resistant lymphocyte subsets, two-colour immunofluorescence tests were conducted in the liver and spleen. NKT cells were found to be such cells in the liver of young mice. On the other hand, an infiltration of granulocytes due to stress was more prominent in the liver of old mice than in young mice. Liver injury as a result of stress was prominent in young mice. This age-related bias in the function of NKT cells and granulocytes seemed to be associated with a difference in the responses of catecholamines (high in old mice) and corticosterone (high in young mice) after stress. Indeed, an injection of adrenaline mainly induced the infiltration of granulocytes while that of cortisol activated NKT cells. The present results suggest the existence of age-related bias in the function of NKT cells and granulocytes after stress and that such bias might be produced by different responses of sympathetic nerves and steroid hormones between young and old mice.
authors.affiliation: Department of Immunology, Niigata University School of Medicine, Niigata, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sagiyama
authors.forename: M
authors.initials: M
authors.lastname: Tsuchida
authors.forename: H
authors.initials: H
authors.lastname: Kawamura
authors.forename: S
authors.initials: S
authors.lastname: Wang
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: X
authors.initials: X
authors.lastname: Bai
authors.forename: T
authors.initials: T
authors.lastname: Nagura
authors.forename: S
authors.initials: S
authors.lastname: Nozoe
authors.forename: T
authors.initials: T
authors.lastname: Abo
mesh_terms: D000375:Aging / Q000276:immunology*; D000818:Animals; D003602:Cytotoxicity, Immunologic; D004837:Epinephrine / Q000494:pharmacology; D006098:Granulocytes / Q000276:immunology*; D006854:Hydrocortisone / Q000031:analogs & derivatives* / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000276:immunology*; D008099:Liver / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D016131:Lymphocyte Subsets / Q000276:immunology; D008221:Lymphoid Tissue / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D012149:Restraint, Physical; D013154:Spleen / Q000276:immunology; D013312:Stress, Physiological / Q000276:immunology*; D013564:Sympathetic Nervous System / Q000276:immunology
chemical_list: C007133:hydrocortisone hemisuccinate; D006854:Hydrocortisone; D004837:Epinephrine