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Cold restraint (CR) for 1 h elicits a psychological and physiological stress that inhibits host defenses against Listeria monocytogenes (LM). Previous analyses indicated that this inhibition is not due to depletion of B or T cells but is instead dependent on signaling through beta-adrenoceptors (betaARs). We now show that impaired host resistance by CR cannot be accounted for by a decrease in LM-specific (listeriolysin O(91-99) tetramer(+)) effector CD8(+) T cells; this result is consistent with previous observations that CR-induced effects are mainly limited to early anti-LM responses. beta2-Adrenoceptor (beta2AR)(-/-) FVB/NJ and wild-type FVB/NJ mice had equivalent anti-LM defenses, whereas beta1-adrenoceptor (beta1AR)(-/-) FVB/NJ mice had lower levels of LM even when subjected to CR treatment. Additionally, host-resistance competency of beta1AR(-/-) mice could be transferred to irradiated wild-type mice reconstituted with beta1AR(-/-) bone marrow progenitors and spleen cells, indicating that beta1AR signaling on immune cells reduces anti-LM responses. beta1AR(-/-) mice had improved cellular (delayed-type hypersensitivity) responses while beta2AR(-/-) mice had improved humoral responses (IgG1, IgG2, and IgM), a result that further explains the strain differences in LM defenses. CR-induced expression of beta1AR and beta2AR mRNA was assessed by real-time PCR. CR treatment significantly increased betaAR mRNAs in Ficoll-purified and F4/80(+)-enhanced liver but not splenic homogenates, demonstrating an organ-specific effect of stress that alters host defenses. Finally, CR treatment induced early increases in perforin expression that may enhance immune cell apoptosis and interfere with LM clearance. In conclusion, beta1AR signaling has immunomodulatory effects on early cell-mediated immune responses; a lack of beta1AR signaling improves antilisterial defenses and cell-mediated immunity, in general.

β1-Adrenergic Receptors on Immune Cells Impair Innate Defenses against Listeria