ENDOGENOUS GAMMA-INTERFERON, TUMOR-NECROSIS-FACTOR, AND INTERLEUKIN-6 IN STAPHYLOCOCCUS-AUREUS INFECTION IN MICE
ENDOGENOUS GAMMA-INTERFERON, TUMOR-NECROSIS-FACTOR, AND INTERLEUKIN-6 IN STAPHYLOCOCCUS-AUREUS INFECTION IN MICE
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DOI：
10.1128/iai.63.4.1165-1172.1995
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发表时间：
1995-04-01
影响因子：
3.1
通讯作者：
MINAGAWA, T
中科院分区：
文献类型：
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作者：
NAKANE, A;OKAMOTO, M;MINAGAWA, T
研究了螨体内内源性γ干扰素（IFN-γ）、肿瘤坏死因子（TNF）和白细胞介素-6（IL-6）在金黄色葡萄球菌致死性和非致死性感染中的产生和作用。在非致死性感染的情况下，虽然在血流中没有检测到细菌，但在肾脏中发现了持续定植和增殖3周的细菌。所有接受致命注射的小鼠都在7天内死亡，在血液、脾脏和肾脏中检测到大量细菌。IFN-γ、TNF和IL-6在非致死性和致死性感染小鼠的血流和脾脏中在24 h内观察到第一个峰值。此后，在非致死性病例中，IFN-γ、TNF和IL-6在肾脏中细菌最大生长期间再次在脾脏和肾脏中达到峰值，尽管在血清中仅检测到IL-6。相反，在致死性感染的情况下，血清中IFN-γ和IL-6的滴度以及肾脏中TNF的滴度在死亡前达到峰值。体内应用抗IFN-γ和TNF单克隆抗体对S.金黄色葡萄球菌感染的小鼠进行了研究。在非致死性感染中，抗TNF α（抗TNF-α）单抗处理的小鼠，而不是抗IFN-γ单抗处理的小鼠，由于感染恶化而死亡，表明内源性TNF在宿主对S.金黄色葡萄球菌感染在接受致死剂量的小鼠中，注射抗TNF-α单克隆抗体加速了死亡。然而，尽管注射抗IFN-γ单克隆抗体在感染早期抑制了感染小鼠的宿主抵抗力，但大多数动物通过注射抗IFN-γ单克隆抗体而在致死感染中存活，这表明内源性IFN-γ在S.金黄色葡萄球菌感染。因此，本研究表明IFN-γ和TNF在S.金黄色葡萄球菌感染
The production and roles of endogenous gamma interferon (IFN-gamma), tumor necrosis factor (TNF), and interleukin-6 (IL-6) in both lethal and nonlethal infections of Staphylococcus aureus were investigated in mite. In the case of nonlethal infection, although no bacteria were detected in the bloodstreams, bacteria that colonized and proliferated persistently for 3 weeks were found in the kidneys. All mice given lethal injections died within 7 days, and large numbers of bacteria were detected in the bloodstreams, spleens, and kidneys. The first peaks of IFN-gamma, TNF, and IL-6 were observed in the bloodstreams and spleens of the mice with nonlethal and lethal infections within 24 h. Thereafter, in the nonlethal cases, IFN-gamma, TNF, and IL-6 peaked again in the spleens and kidneys during the period of maximum growth of bacteria in the kidneys, although only IL-6 was detected in the sera. In contrast, in the case of lethal infection, the titers of IFN-gamma and IL-6 in the sera and TNF in the kidneys peaked before death. Effects of in vivo administration of monoclonal antibodies (MAbs) against IFN-gamma and TNF on the fates of S. aureus-infected mice were studied. In the nonlethal infections, anti-TNF alpha (anti-TNF-alpha) MAb-treated mice, but not anti-IFN-gamma MAb-treated mice, died as a result of worsening infection, suggesting that endogenous TNF plays a protective role in host resistance to S. aureus infection. In the mice that received lethal doses, injection of anti-TNF-alpha MAb accelerated death. However, although injection of anti-IFN-gamma MAb inhibited host resistance of the infected mice early in infection, most of the animals survived the lethal infection by injection of anti-IFN-gamma MAb, suggesting that endogenous IFN-gamma plays a detrimental role in S. aureus infection. Thus, this study demonstrated that IFN-gamma and TNF play different roles in S. aureus infection.