ToxSci Advance Access published online on May 28, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg146
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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1 Laboratory of Clinical and Environmental Endocrinology and Immunology, Wadsworth Center, New York State Department of Health, Albany, NY
* To whom correspondence should be addressed. E-mail: david.lawrence{at}wadsworth.org.
Experiments were conducted to delineate the cellular changes modulated by acute cold/restraint stress (ACRS), a physical and psychological stressor, in response to a Listeria monocytogenes (LM) infection. In addition to wild-type (WT) BALB/c mice, CD4 deficient (CD4-/-) BALB/c mice, which have no effective adaptive immunity, were used to determine the involvement of adaptive versus innate immunity. ACRS-induced suppression of host resistance to LM was not observed in CD4-/- mice, suggesting the involvement of CD4+ T cells in the ACRS-induced inhibition. The in vivo splenic leukocyte phenotypes and activities of WT BALB/c mice after infection and in vitro lymphocyte responses to heat-killed LM (HKLM) also were examined. There were no significant differences in the numbers of splenic T and B lymphocytes, natural killer (NK) cells, macrophages or neutrophils between non-stressed and ACRS-treated WT mice. However, higher levels of activated T cells and non-T lymphocytes were observed in the ACRS-treated mice;
© 2003 Society of Toxicology
Immunotoxicology
Immune Changes During Acute Cold/Restraint Stress-Induced Inhibition of Host Resistance to Listeria
Abstract 
-adrenergic receptor (-ADR) antagonists (propranolol and atenolol) eliminated these elevated levels of activation as well as the ACRS-induced suppression of host resistance. ACRS and control mice also had equivalent activation of macrophages. With in vitro HKLM stimulation, splenocytes from ACRS-treated mice produced significantly higher levels of IFN
and slightly higher levels of IL-6 in comparison to the non-stressed mice although equivalent levels of lymphocyte proliferation were obtained. Additionally, ACRS-treated mice showed comparable elevation of serum nitric oxide (NO) after infection, indicating macrophage bactericidal activity similar to non-stressed mice. Thus, it appears that ACRS inhibits host resistance through regulatory CD4+ T cells and/or effector cell functions downstream of CD4+ T cell activation as well as through -ADR signaling, in that blockage of these receptors appears to aid host defenses by means other than elevation of helper T cell activity. Since CD4 T cell deficiency and -ADR blockage produced equivalent effects, -ADR+ CD4+ T cells may have a negative role on host defenses after ACRS.
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