The crosstalk of immune system and nerve system in host defense to bacterial infections

免疫系统和神经系统之间的相互作用被认为与体内平衡有关。我们从神经肽、交感神经系统、宿主防御和细胞因子产生相互作用的角度研究了这些系统在单核增生李斯特菌（LM）感染小鼠模型中的串扰我们研究了P物质（SP）和血管活性肠肽（VIP）等神经肽对热杀伤LM （HK-LM）诱导的脾细胞生成ifn - γ和tnf - α的影响。两种神经肽都不影响这些细胞因子的产生。接下来，为了了解神经肽的自分泌和旁分泌作用，我们在培养物中加入了抗SP和VIP的抗体。两种抗体均不影响ifn - γ和tnf - α 2的产生我们研究了体内注射α -黑色素细胞刺激激素（α - msh）对LM感染和细胞因子产生的影响。2 . α - msh对HK-LM诱导的脾细胞抗李斯特菌防御及ifn - γ和tnf - α的产生无显著影响6-羟多巴胺（6-OHDA）可破坏去甲肾上腺素能神经末梢，当小鼠预先接受6-羟多巴胺（6-OHDA）处理时，宿主对LM的防御在感染后期增强。用地西帕明预处理可以阻止6-羟色胺进入神经纤维我们研究了6-OHDA去神经对小鼠脾脏LM感染诱导的内源性ifn - γ、tnf - α和IL-12产生的影响。未观察到去神经支配对内源性细胞因子产生的影响。然而，在6- ohda预处理小鼠的脾细胞培养中，HK-LM诱导的tnf - α产生和anti-CD3 mAb诱导的ifn - γ产生增强。我们的研究结果表明，宿主对LM感染的防御以及在防御中至关重要的ifn - γ和tnf - α的产生通过交感神经系统的阻断而增强，这表明宿主对LM感染的防御可能依赖于免疫系统和神经系统之间的相互作用。少

The crosstalk between immune system and nerve system is known to be involved in homeostasis. We studied the crosstalk betwwen these to systems in Listeria monocytogenes (LM)-infected mouse model from the standpoints of the interactions between neuropeptides, sympathetic nerve system, host defense, and cytokine production.1 We investigated the effects of neuropeptides such as substance P (SP) and vasoactive intestinal peptide (VIP) on IFN-gamma and TNF-alpha production induced by heat-killed LM (HK-LM) in spleen cell cultures obtained from naive mice and LM-immunized mice. Neither neuropeptides affected the productions these cytokines. Next, to know the autocrine and paracrine actions of neuropeptides, antibodies against SP and VIP were added the cultures. Neither antibodies affected on the productions of IFN-gamma and TNF-alpha.2 We investigated the effects of in vivo administration of alpha-melanocyte-stimulating hormone (alpha-MSH) on LM infection and cytokine production. No signific … More ant effect of alpha-MSH on antilisterial defense and the productions of IFN-gamma and TNF-alpha induced by HK-LM in spleen cell cultures.3 When mice was pretreated with 6-hydroxydopamine (6-OHDA), which destroys noradrenergic nerve terminals, host defense to LM was augmented late in infection. This effect was prevented by pretreatment with desipramine, which blocks the uptake of 6-OHDA into the nerve fibers.4 We inverstigated the effects of denervation by 6-OHDA on endogenous IFN-gamma, TNF-alpha, and IL-12 production induced by infection with LM in the spleens of mice. No effect of denervation on endogenous cytokine production was observed. However, TNF-alpha production induced by HK-LM and IFN-gamma production induced by anti-CD3 mAb was enhanced in spleen cell cultures obtained from 6-OHDA-pretreated mice.Our results demonstrated that host defense to LM infections and the productions of IFN-gamma, and TNF-alpha, which are crucial in the defense, were augmented by block of the sympatheic nerve system, suggesting that host defense to LM infection might be depend on the interactions between immune system and nerve system. Less