| First Author | Bilbo SD | Year | 2003 |
| Journal | J Neuroimmunol | Volume | 140 |
| Issue | 1-2 | Pages | 41-8 |
| PubMed ID | 12864970 | Mgi Jnum | J:119000 |
| Mgi Id | MGI:3700911 | Doi | 10.1016/s0165-5728(03)00175-9 |
| Citation | Bilbo SD, et al. (2003) Blunted stress responses in delayed type hypersensitivity in mice lacking the neuronal isoform of nitric oxide synthase. J Neuroimmunol 140(1-2):41-8 |
| abstractText | 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. |
