The control of bacterial infectious diseases by the orchestra of immune system and nerve system

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The intimate interaction between immune system and nerve system is known to be involved in homeostasis. We studied the orchestra betwwen these two systems in Listeria monocytogenes-infected mouse model in which the sympathetic system, especially noradrenergic nerve terminals, is destroyed by administration of 6-hydroxydopamine (6-OHDA).(1) When mice was pretreated with 6-OHDA), host defense to L.monocytogenes infection was augmented late in infection. This effect was prevented by pretreatment with desipramine, which blocks the uptake of 6-OHDA into the nerve fibers.(2) We investigated the effect of denervation by 6-OHDA on phagocytic, listericidal, and NO production by splenic macrophages and peritoneal macrophages. However, activation of either macrophages was not observed.(3) We investigated the effect of denervation by 6-OHDA on T-cell-dependent antilisterial resistance by depletion of T-cell subsets in vivo. Augmentation of the resistance by denervation was abolished by depletion of CD8 T cells, suggesting that CD8 T cells are involved in this phenomenon.(4) We investigated the effect of denervation by 6-OHDA on cytokine production by splenic dendritic cells. IL-12, TNF-α and IFN-γ production induce by heat killed L.monocytogenes was augmented, suggesting that IL-12-mediated induction of T-helper 1 polarization by dendritic cells might be involved in augmentation of antilisterial resistance by denervation.(5) We also investigated the role of adrenergic receptors on host defense to L.monocytogenes infection. Administration of α-adrenergic receptor antagonists, but not β-adrenergic receptor antagonists, inhibited antilisterial resistance, suggesting that α-adrenergic receptors are involved in host defense to L.monocytogenes infection.Our results demonstrated that the intimate interactions between immune system and nerve system might be required to control L.monocytogenes infection.