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Protective Role of Interleukin-6 during Yersinia enterocolitica Infection Is Mediated through the Modulation of Inflammatory Cytokines

机译:白细胞介素6在小肠结肠炎耶尔森氏菌感染中的保护作用是通过调节炎症细胞因子介导的。

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Yersinia enterocolitica is a gram-negative enteric pathogen responsible for a number of gastrointestinal disorders. A striking feature of the pathology of a Y. enterocolitica infection is inflammation. Recently, we demonstrated a role for interleukin-1α (IL-1α) in the establishment of intestinal inflammation in response to a Y. enterocolitica infection. A cytokine directly affected by IL-1 levels is IL-6. A previous report suggested that IL-6 plays an anti-inflammatory role during Y. enterocolitica infection, and in other systems IL-6 has been shown to be proinflammatory. Therefore, a closer examination of the roles of IL-6 and inflammatory cytokines in the control of Y. enterocolitica infection in IL-6?/? mice was undertaken. Y. enterocolitica organisms were more virulent in the IL-6?/? mice (60-fold decreased 50% lethal dose) and colonized systemic tissues more rapidly and to a higher level than in the wild-type mice. One role of IL-6 during a Y. enterocolitica infection may be the downmodulation of the inflammatory response. The IL-6?/? mice have a more robust TH1 T-cell response, as well as hyperinflammatory pathologies. These phenotypes appear to be due to the misregulation of tumor necrosis factor alpha, monocyte chemotactic protein 1, IL-10, transforming growth factor β1, and gamma interferon in the IL-6?/? mouse. These data provide further insight into the intricate cytokine signaling pathways involved in the regulation of inflammatory responses and the control of bacterial infections.
机译:肠球菌耶尔森氏菌是一种革兰氏阴性肠病原体,可引起多种胃肠道疾病。 Y的病理特征。肠结肠炎感染是炎症。最近,我们证明了白细胞介素1α(IL-1α)在响应 Y的肠道炎症建立中的作用。肠结肠炎感染。直接受IL-1水平影响的细胞因子是IL-6。先前的报道表明IL-6在 Y期间起抗炎作用。肠结肠炎感染以及其他系统中的IL-6已被证明具有促炎作用。因此,仔细检查IL-6和炎性细胞因子在 Y的控制中的作用。在IL-6 ?/?小鼠中进行小肠结肠炎感染。是的IL-6 ?/?小鼠中肠结肠炎菌的毒性更高(50%致死剂量降低了60倍),并且定植的全身组织比野生动物更迅速且水平更高型小鼠。 IL-6在 Y期间的一种作用。肠结肠炎感染可能是炎症反应的下调。 IL-6 ?/?小鼠具有更强的T H 1 T细胞反应,以及高炎症性病理。这些表型似乎是由于IL-6 α/β小鼠中的肿瘤坏死因子α,单核细胞趋化蛋白1,IL-10,转化生长因子β1和γ干扰素的失调引起的。这些数据提供了对参与炎症反应调节和细菌感染控制的复杂细胞因子信号通路的进一步了解。

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