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

探讨了宿主通过儿茶酚胺受体防御细菌感染的机制。此外，巨噬细胞移动抑制因子（macrophagemigrationinhibitoryfactor，MIF）介导免疫系统和神经系统之间的相互作用，在细菌感染中的作用也进行了研究.儿茶酚胺在宿主抵抗细菌感染中的调控机制。研究了肾上腺素受体拮抗剂和激动剂在体内对单核细胞增生李斯特菌感染的宿主防御和细胞因子应答的影响。给小鼠注射肾上腺素受体α拮抗剂后，抗肾上腺素抵抗和IFN-γ、TNF-α的产生受到抑制。相反，表甲肾上腺素受体β拮抗剂对抗真菌药耐药性和细胞因子产生无显著影响。结果提示肾上腺素受体α可能参与调节IFN-γ和TNF-α的产生和抗肿瘤药物的抵抗。MIF在细菌生长中的作用 ...更多信息 感染（1）L.单核细胞增多症给小鼠注射抗MIF抗体对L.然而，这种抗体拯救了小鼠免于单核细胞增多症的致命感染。单核细胞增多症(2)抗MIF抗体处理的小鼠在致死性感染的早期阶段感染器官中内源性IFN-γ和TNF-α的产生上调，但在晚期阶段下调。(3)在抗MIF抗体处理的小鼠中，肝脏中内源性IL-10的产生上调。在抗MIF抗体处理的小鼠中，通过给予抗IL-10抗体，肝功能异常部分恢复。(4)与正常兔球蛋白组相比，MIF抗体组小鼠血浆皮质醇水平显著降低，提示MIF参与了L.单核细胞增生通过调节IL-10的产生。少

The host defense mechanism against bacterial infections through catecholamine receptors was investigated. Furthermore, the role of macrophage migration inhibitory factor (MIF), which is known to mediate the crosstalk between immune system and nerve system, in bacterial infections was investigated.1. The regulatory mechanism by catecholamines in host defense against bacterial infections. The in vivo effects of antagonists and agonists to epinephrine receptors on host defense against Listeria monocytgenes infection and cytokine responses were investigated. When epinephrine receptor α antagonists were injected into mice, antilisterial resistance and productions of IFN-γ and TNF-α were suppressed. In contrast, epimephrine receptor β antagonists revealed no significant effect on antilisterial resistance and the cytokine production. These results suggest that antilisterial resistance and productions of IFN-γ and TNF-α may be regulated by epinephrine receptor α.2. The role of MIF in bacterial … More infections (1) Endogenous MIF levels in the infected organs were up-regulated by a lethal infection with L. monocytogenes. The administration of anti-MIF antibody into mice showed no significant effect on the fate of a sublethal infection with L. monocytogenes, whereas the antibody rescued the mice from a lethal infection with L. monocytogenes. (2) Endogenous IFN-γ and TNF-α production in the infected organs was up-regulated in the early phase but down-regulated in the late phase of lethal infection in anti-MIF antibody-treated mice. (3) Endogenous IL-10 production in the livers was up-regulated in anti-MIF antibody-treated mice. Abnormality of liver function was partially restored by the administration of anti-IL-10 antibody in anti-MIF antibody-treated mice. (4) The level of plasma cortisol was significantly low in anti-MIF antibody-treated mice, compared with that of the normal rabbit globulin-treated mice.These results suggest that MIF is involved in the pathogensis of a lethal infection with L. monocytogenes through the regulation of IL-10 production. Less