Sympathetic nervous system plays a major role in acute cold/restraint stress inhibition of host resistance to Listeria monocytogenes.

BALB/c mice exposed to acute cold/restraint stress (ACRS) had significantly lower host resistance to Listeria monocytogenes (LM) than controls. The stress hormones corticosterone (CORT) and norepinephrine (NE), which are known to modulate immune responses, were evaluated as the cause of the decline in immune defense. The involvement of CORT and NE was investigated by pretreating mice with the CORT synthesis inhibitor metyrapone and the chemical sympathectomy drug 6-hydroxydopamine (6-OHDA), respectively. LM burdens in spleen and liver were determined three days post-infection. 6-OHDA significantly decreased the LM burden in both control and stressed animals. 6-OHDA also completely blocked the stress effects observed in spleens while only partially affecting the liver. The 6-OHDA-uptake inhibitor desipramine aided confirmation that peripheral sympathetic adrenergic nerves and NE depletion, rather than the direct action of 6-OHDA, were responsible for the decreased susceptibility to LM. The results suggest that the peripheral sympathetic nervous system (SNS) postganglionic neurotransmitter NE plays a major role in LM host resistance and has significant tissue-dependent effects after ACRS. In contrast, metyrapone-treated animals had further decreased host resistance to LM, suggesting a potential protective effect of CORT after ACRS. Altogether, the results suggest that stress hormones play an important role in stress-modulated host resistance and that NE is the major hormone involved in ACRS-induced suppression of host resistance.