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Reactive oxygen species inhibits Listeria monocytogenes invasion into HepG2 epithelial cells

机译:活性氧抑制单核细胞增多性李斯特菌侵入HepG2上皮细胞

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Listeria monocytogenes (Lm) can colonize human gastrointestinal tract and subsequently cross the intestinal barrier. Reactive oxygen species (ROS) are produced by NADPH oxidase. However, the role of ROS in bacterial invasion remains to be less understood. Herein, we investigated the impact of ROS on Lm invasion to HepG2 using NADPH oxidase inhibitor, diphenyleneiodonium chloride (DPI), as well as the ROS scavenger, N ‐acetyl cysteine (NAC). Our results showed that inhibiting ROS increased the invasive capability of Lm. Moreover, after Lm infection, inflammatory cytokines such as tumor necrosis factor alpha (TNF‐α) and interleukin 1beta (IL‐1β) in HepG2 were significantly upregulated. However, after inhibiting ROS, the expression levels of TNF‐α and IL‐1β were downregulated, indicating a failure of host cells to activate the immune mechanism. Taken together, ROS in Lm might be as a signal for host cells to sense Lm invasion and then stimulate cells to activate the immune mechanism.
机译:单核细胞增生性李斯特菌(Lm)可以在人的胃肠道定居,并随后穿过肠道屏障。 NADPH氧化酶可产生活性氧(ROS)。然而,ROS在细菌入侵中的作用尚不清楚。在本文中,我们使用NADPH氧化酶抑制剂二苯二碘氯化铵(DPI)和ROS清除剂N-乙酰半胱氨酸(NAC)研究了ROS对Lm侵袭HepG2的影响。我们的结果表明,抑制ROS可以增加Lm的侵袭能力。此外,Lm感染后,HepG2中的炎症细胞因子(如肿瘤坏死因子α(TNF-α)和白介素1beta(IL-1β))显着上调。然而,在抑制ROS后,TNF-α和IL-1β的表达水平被下调,表明宿主细胞不能激活免疫机制。综上所述,Lm中的ROS可能是宿主细胞感知Lm入侵并随后刺激细胞激活免疫机制的信号。

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