Tumor necrosis factor-independent IL-6 production during murine listeriosis.
Tumor necrosis factor-independent IL-6 production during murine listeriosis.
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DOI：
10.4049/jimmunol.146.2.756
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发表时间：
1991-01
影响因子：
4.4
通讯作者：
E. A. Havell;P. Sehgal
中科院分区：
文献类型：
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作者：
E. A. Havell;P. Sehgal
我们报告，TNF，IL-6和IFN-α/β产生的小鼠在亚致死或致死单核细胞增生李斯特菌感染。这些细胞因子在感染的脾脏中的数量增加和减少与这些器官中的细菌数量一致。虽然所有这些细胞因子都存在于李斯特菌感染的脾脏中，但在外周循环中仅发现IL-6和IFN-α/β。由于已经报道TNF负责在接种致死剂量的革兰氏阴性细菌大肠杆菌（Escherichia coli）后体内产生IL-6（Fong等人，1989. J. Exp. 170：1627），进行实验以确定革兰氏阳性细菌L.单核细胞增多症，也是TNF依赖性的。发现在静脉内注射致死或亚致死李斯特菌接种物之前不久用TNF特异性中和抗体对小鼠进行被动免疫导致内源性产生的TNF的完全中和，以及感染器官中细菌的逐步增殖。还发现抗TNF IgG处理导致存在于脾和血液中的李斯特菌诱导的IL-6的量的进行性增加，直到宿主死亡。这些发现表明，李斯特菌诱导的小鼠IL-6产生主要通过TNF非依赖性途径发生，并与感染的严重程度直接相关。
We report that TNF, IL-6, and IFN-alpha/beta are produced by mice during either sublethal or lethal Listeria monocytogenes infections. The quantities of these cytokines in infected spleens increase and decrease in concordance with bacterial numbers in these organs. While all of these cytokines were present in Listeria-infected spleens, only IL-6 and IFN-alpha/beta were found in the peripheral circulation. Inasmuch as TNF has been reported to be responsible for the production of IL-6 in vivo following the inoculation of a lethal dose of the Gram-negative bacterium, Escherichia coli (Fong et al., 1989. J. Exp. Med. 170: 1627), experiments were undertaken to determine whether IL-6 production elicited by the Gram-positive bacterium, L. monocytogenes, was also TNF-dependent. It was found that the passive immunization of mice with neutralizing antibodies specific for TNF shortly before i.v. injection of a lethal or sublethal Listeria inoculum resulted in the complete neutralization of endogenously produced TNF, and in the progressive multiplication of bacteria in infected organs. It was also found that the anti-TNF IgG treatment resulted in a progressive increase in the amounts of Listeria-induced IL-6 present in spleen and blood, until the death of the host. These findings indicate that Listeria-induced IL-6 production in mice occurs primarily through a TNF-independent pathway, and correlates directly with the severity of the infection.