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首页> 外文期刊>Infection and immunity >Association between virulence of Yersinia pestis and suppression of gamma interferon and tumor necrosis factor alpha.
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Association between virulence of Yersinia pestis and suppression of gamma interferon and tumor necrosis factor alpha.

机译：鼠疫耶尔森氏菌毒力与γ干扰素和肿瘤坏死因子α抑制之间的关联。

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It is established that Yersinia pestis, the causative agent of bubonic plague, and enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica share a ca. 70-kb low-calcium response or Lcr plasmid (Lcr+). The latter is known to encode regulatory functions that restrict growth at 37 degrees C in Ca(2+)-deficient medium and virulence factors that are expressed only in vitro within this environment (e.g., certain Yops and V antigen). In this study, gamma interferon (IFN-gamma) was never detected in mice infected with 10 minimum lethal doses (MLD) of Lcr+ cells of Y. pestis, and significant levels of tumor necrosis factor alpha (TNF-alpha) arose only prior to death. Prompt and marked synthesis of these cytokines was observed upon infection with avirulent Lcr- mutants. Treatment of mice with exogenous IFN-gamma plus TNF-alpha inhibited multiplication of Lcr+ yersiniae in vivo, thereby providing protection against challenge with 10 MLD. Administration of both cytokines was required for absolute survival, suggesting a synergistic rather than cumulative interaction. This protective effect entailed cytokine priming as judged by subsequent detection of substantial levels of endogenous IFN-gamma and TNF-alpha. Monospecific anti-V-antigen, known to provide passive immunity against 10 MLD of Lcr+ Y. pestis, permitted significant synthesis of endogenous IFN-gamma and TNF-alpha. These findings demonstrate that Lcr+ yersiniae suppress synthesis of cytokines and suggest that this effect is mediated by one or more Lcr plasmid-encoded virulence factors.
机译：已经确定，鼠疫鼠疫耶尔森氏菌与肠致病性耶尔森氏菌假结核耶尔森氏菌和肠小肠结肠炎耶尔森氏菌共享ca。 70-kb低钙应答或Lcr质粒（Lcr +）。已知后者编码调节功能，该功能限制在Ca（2+）缺乏的培养基中在37摄氏度下的生长和仅在该环境中体外表达的毒力因子（例如某些Yops和V抗原）。在这项研究中，从未在鼠疫耶尔森氏菌Lcr +细胞的10个最小致死剂量（MLD）感染的小鼠中检测到γ干扰素（IFN-γ），并且仅在之前才出现了显着水平的肿瘤坏死因子α（TNF-alpha）。死亡。在用无毒的Lcr突变体感染后，观察到这些细胞因子的迅速和明显的合成。用外源IFN-γ加TNF-α治疗小鼠在体内抑制了Lcr +耶尔森氏菌的繁殖，从而提供了针对10 MLD攻击的保护。绝对生存需要同时使用两种细胞因子，这表明存在协同作用而不是累积相互作用。通过随后检测到大量内源性IFN-γ和TNF-α来判断，这种保护作用需要引发细胞因子。已知可提供针对Lcr +鼠疫杆菌的10 MLD的被动免疫的单特异性抗V抗原，可大量合成内源性IFN-γ和TNF-α。这些发现表明，Lcr +耶尔森氏菌抑制细胞因子的合成，并表明这种作用是由一种或多种Lcr质粒编码的毒力因子介导的。

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