| First Author | Manfredi B | Year | 1998 |
| Journal | Brain Behav Immun | Volume | 12 |
| Issue | 3 | Pages | 201-11 |
| PubMed ID | 9769156 | Mgi Jnum | J:50868 |
| Mgi Id | MGI:1312990 | Doi | 10.1006/brbi.1998.0525 |
| Citation | Manfredi B, et al. (1998) IL-6 knock-out mice show modified basal immune functions, but normal immune responses to stress. Brain Behav Immun 12(3):201-11 |
| abstractText | To better determine the role of interleukin-6 in the mechanisms that regulate stress-induced immunosuppression, we used in this study an interleukin-6-deficient mice model recently generated by gene targeting. We report here that, in basal conditions, mutant mice are characterized by altered immune functions. Natural killer activity and interleukin-2 production are lower in splenocytes of interleukin-6 deficient mice compared to those of controls, whereas Concanavalin A-induced splenocyte proliferation is comparable with that observed in wild-type mice. Moreover, splenocyte concentrations of the immunosuppressive opioid peptide beta-endorphin are higher in interleukin-6 deficient mice while serum corticosterone concentrations are unchanged. After exposure to 16 h of restraint stress, a significant suppression of the immune parameters is exhibited and a significant increase of splenocyte beta-endorphin concentrations are present in knock-out and normal animals. Finally, corticosterone is normally induced in stressed interleukin-6-deficient mice, thus demonstrating that interleukin-6 is not crucial for the activation of the hypothalamic-pituitary-adrenal axis. In conclusion, our results indicate that interleukin-6 is not a key factor in the immunosuppression observed after restraint stress. Copyright 1998 Academic Press. |
