Blunted stress responses in delayed type hypersensitivity in mice lacking the neuronal isoform of nitric oxide synthase.

Published

Journal Article

Nitric oxide (NO) is implicated in inflammation and hypothalamic-pituitary responses to immune stimuli; however, the specific role of NO from neurons during stress-induced immune responses remains unspecified. We measured antigen-specific delayed-type-hypersensitivity (DTH) responses in the skin of wild-type (WT) and neuronal nitric oxide synthase knockout (nNOS(-/-)) mice at baseline and after 2 h of restraint. Baseline corticosterone concentrations were higher in nNOS(-/-) than WT mice. However, stress-induced increases in corticosterone were dampened in nNOS(-/-) mice, and restraint suppressed DTH only in WT animals. Furthermore, WT mice lost more body mass after stress, and exhibited more anxiety-like behavior in the open field, than nNOS(-/-) mice. Neuronal NO appears to be involved in the neuroendocrine-immune response to stress, perhaps via glucocorticoid regulation.

Full Text

Cited Authors

  • Bilbo, SD; Hotchkiss, AK; Chiavegatto, S; Nelson, RJ

Published Date

  • July 2003

Published In

Volume / Issue

  • 140 / 1-2

Start / End Page

  • 41 - 48

PubMed ID

  • 12864970

Pubmed Central ID

  • 12864970

Electronic International Standard Serial Number (EISSN)

  • 1872-8421

International Standard Serial Number (ISSN)

  • 0165-5728

Digital Object Identifier (DOI)

  • 10.1016/s0165-5728(03)00175-9

Language

  • eng