Journal Article

Immune Changes during Acute Cold/Restraint Stress-Induced Inhibition of Host Resistance to <i>Listeria</i>

Ling Cao, Chad A. Hudson and David A. Lawrence

in Toxicological Sciences

Volume 74, issue 2, pages 325-334
Published in print August 2003 | ISSN: 1096-6080
Published online August 2003 | e-ISSN: 1096-0929 | DOI: http://dx.doi.org/10.1093/toxsci/kfg146
Immune Changes during Acute Cold/Restraint Stress-Induced Inhibition of Host Resistance to Listeria

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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 acute cold/restraint stress (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 cells, macrophages, or neutrophils between nonstressed and ACRS-treated WT mice. However, higher levels of activated T cells and non-T lymphocytes were observed in the ACRS-treated mice; β-adrenergic receptor (β-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 IFNγ and slightly higher levels of IL-6 in comparison with the nonstressed mice, although equivalent levels of lymphocyte proliferation were obtained. Additionally, ACRS-treated mice showed comparable elevation of serum nitric oxide after infection, indicating macrophage bactericidal activity similar to nonstressed 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 β-ADR signaling, in that blockage of these receptors appears to aid host defenses by means other than elevation of helper T cell activity. Because CD4 T cell deficiency and β-ADR blockage produced equivalent effects, β-ADR+ CD4+ T cells may have a negative role on host defenses after ACRS.

Keywords: acute cold/restraint stress; host resistance; Listeria monocytogenes; CD4/mice; nitric oxide

Journal Article.  6895 words.  Illustrated.

Subjects: Medical Toxicology ; Toxicology (Non-medical)

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