Effects of Rotational Stress of Different Duration on NK Cell Activity, Proinflammatory Cytokines, and POMC-Derived Peptides in Mice

Abstract

Previous studies have shown that the same stressor, depending on intensity, controllability, or duration, can have different effects on the immune system. The purpose of this study was to determine the effect of 10- and 20-min rotation on natural killer (NK) cell activity and also to establish if changes in body temperature, proinflammatory cytokine (IL-1β, IL-6, and TNF-α) levels, and proopiomelanocortin (POMC)-derived peptide (ACTH and β-endorphin) levels parallel the changes in NK cell activity in mice. We found that 10-min rotation significantly increased NK cell activity as compared to both the control (home cage) group and the 20-min-rotation group, while NK cell activity in the 20-min group was not significantly changed compared to the control group. Both 10 and 20 min of rotational stress decreased body temperature and induced significant changes in the proinflammatory cytokine and POMC-derived peptide levels as compared to the control group. The pattern of proinflammatory cytokine expression was quite different between the 10- and 20-min rotation groups. All three proinflammatory cytokines were expressed sequentially (at 0 h after rotation TNF-α, at 6 h IL-1β and IL-6, and at 24 h IL-6) in the 10-min rotation group, while the 20-min rotation group had a small increase in IL-1β (6.7 ± 1.8 pg/ml) at 0 h and increased levels of IL-6 at 6 and 24 h. There was a dissociation of ACTH and β-endorphin expression in both groups resulting in significantly more β-endorphin (p < 0.05) in the 10-min group at 6 h and significantly more ACTH (p < 0.04) in the 20-min group at 6 h. IL-1β and β-endorphin have both been shown to have a direct stimulatory effect on NK cell activity. Therefore, we suspect that the significant increase in both IL-1β and β-endorphin at 6 h in the 10-min-rotation group may be involved in the increased NK cell activity observed at 24 h in the 10-min-rotation group.

Enhanced Recovery of NK Cell Activity in Mice under Restraint Stress by the Administration of a Biological Response Modifier Derived from the Mycelia of the Basidiomycete Tricholoma matsutake

“…Furthermore, because CM6271 had no clear effect on the changes caused by restraint in the blood levels of immunosuppressive corticosterone or in the lipid peroxide level in the liver, it is suggested that actions on the immune system through direct action on the endocrine system and the oxidation-reduction system are unlikely. In relation to a possible mode of action, mediated by the immune system, for the effect of CM6271 on NK cell activity, we observed no effect on the blood levels of cytokines IL-6 and TNF-a, whose production is reported to be altered by stress loading (Hale et al, 2001;Nukina et al, 2001).…”

Exposure to acute physical and psychological stress alters the response of rat macrophages to corticosterone, neuropeptide Y and beta-endorphin

“…BE is primarily synthesised in the hypothalamus and the anterior and intermediate lobes of the pituitary (Stratakis and Chrousos 1995;Smith and Funder 1988), but also in monocytes, granulocytes, lymphocytes and macrophages (Mousa et al 2004). Stress significantly increases the BE concentration in plasma and within immune cells (Sacerdote et al 1994;Tsukada et al 2001), which together could contribute to stressinduced immunomodulation (Hale et al 2001).…”

Corticosterone Changes in Response to Stressors, Acute and Protracted Actions of Tumor Necrosis Factor-α, and Lipopolysaccharide Treatments in Mice Lacking the Tumor Necrosis Factor-α p55 Receptor Gene

“…Given that TNF-· may also contribute to the neuroendocrine effects elicited by the bacterial endotoxin, lipopolysaccharide (LPS) [16], the role of p55 was also investigated in this respect. Finally, since psychogenic stressors have been reported to increase TNF-· levels [17], coupled with the finding that other cytokines such as IL-1 have been implicated in immobilization-induced HPA activation. [18], it was of interest to determine whether p55 contributes to HPA activation elicited by a restraint or auditory stressor.…”