Regulatory effect of interleukin-4 in the innate inflammatory response to rhodococcus aurantiacus infection in mice.
Regulatory effect of interleukin-4 in the innate inflammatory response to rhodococcus aurantiacus infection in mice.
复制标题
IL-4 对小鼠金黄色红球菌感染先天炎症反应的调节作用。
DOI：
10.1089/jir.2014.0107
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Watanabe M
中科院分区：
文献类型：
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作者：
Yimin;Kohanawa M;Zhao S;Li M;Kuge Y;Tamaki N;Watanabe M
白细胞介素-4促进橙色红球菌感染晚期肉芽肿消退在这项研究中，使用IL-4缺陷小鼠研究了IL-4对针对该细菌的初始应答的贡献。与野生型（WT）小鼠相比，IL-4缺陷小鼠在感染的初始阶段显示出显著降低的肝、脾和血液中肿瘤坏死因子（TNF）-α和IL-6的分泌，沿着存活率的提高。IL-4缺陷小鼠还显示脾脏和血液中IL-10分泌减少;然而，肝脏IL-10水平与WT动物中观察到的水平相似，并且伴随着早期感染阶段肝脏中干扰素（IFN）-γ产生增加和细菌负荷降低。组织学检查显示，感染的IL-4缺陷小鼠肝肉芽肿形成减少。在挑战与热killedr。与WT小鼠细胞相比，IL-4缺陷型小鼠巨噬细胞在基因和蛋白水平上均显示TNF-α、IL-6和IL-10的表达降低。这些结果表明，在启动的R。在橙黄引起的炎症中，IL-4缺乏减弱巨噬细胞中的细胞因子应答，这有助于改善小鼠存活和减少肉芽肿性炎症，并增强肝脏IFN-γ应答，其短暂加速细菌消除。
Interleukin (IL)-4 promotes the regression of granulomas during the late phase ofRhodococcus aurantiacusinfection. In this study, the contribution of IL-4 to the initial response against this bacterium was investigated using IL-4-deficient mice. Compared with wild-type (WT) mice, IL-4-deficient mice displayed remarkably lower tumor necrosis factor (TNF)-α and IL-6 secretion in the liver, spleen, and blood at the initial phase of infection, along with improved survival. IL-4-deficient mice also showed diminished IL-10 secretion in the spleen and blood; however, hepatic IL-10 levels were similar to those observed in WT animals, and were concomitant with augmented interferon (IFN)-γ production and decreased bacterial burden in the liver at the early infection phase. Histological examination revealed reduced hepatic granuloma formation in infected IL-4-deficient mice. On challenge with heat-killedR. aurantiacus, IL-4-deficient mouse macrophages showed reduced expression of TNF-α, IL-6, and IL-10 at both the gene and protein levels compared with WT mouse cells. These findings indicate that during the initiation ofR. aurantiacus-induced inflammation, IL-4 deficiency attenuates cytokine responses in macrophages, which contributes to amelioration in mouse survival and reduction of granulomatous inflammation, and augments a hepatic IFN-γ response which transiently accelerates bacterial elimination.