Stress-induced extracellular Hsp72 is a functionally significant danger signal to the immune system.

摘要: Extracellular heat-shock proteins (eHsp) such as those belonging to the 70-kDa family of Hsp (eg, Hsp72) have been hypothesized act a "danger signal" immune cells, promote responses, and improve host defense. The current study tested this hypothesis. Adult male F344 rats were exposed an acute laboratory stressor (100, 5-second, 1.6-mA inescapable tail shocks) challenged with Escherichia coli. number colony-forming units (CFU) bacteria at site injection, levels eHsp72, response eHsp72 E. coli-derived lipopolysaccharide (LPS), amount time required recover from in vivo bacterial challenge measured. CFUs reduced 2, 4, 6 hours after injection coli stress. Rats stress had elevated that was rapidly (25 minutes) remained circulation inflammatory (2 termination). Both exposure administration absence resulted facilitated pattern recovery inflammation induced by subcutaneous injection. restraint (100 did not demonstrate circulating or challenge. In vitro stimulation rat splenocytes macrophages nitric oxide (NO), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, effect specific because it diminished polymyxin B earlier heat-denature treatment. Stimulation cells combined LPS greater NO cytokine than observed alone. vivo, site, bacterial-induced potentiated stress, inhibition (L-NIO) stress-induced facilitation but no on control kinetics recovery. Thus, these results lend support hypothesis intense increases which acts danger signal potentiate facilitate inflammation.