The Degree of Helicobacter pylori Infection Affects the State of Macrophage Polarization through Crosstalk between ROS and HIF-1α

The Degree of Helicobacter pylori Infection Affects the State of Macrophage Polarization through Crosstalk between ROS and HIF-1α
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幽门螺杆菌感染程度通过 ROS 和 HIF-1α 之间的串扰影响巨噬细胞极化状态

DOI:
10.1155/2020/5281795
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发表时间:
2020-12-08
影响因子:
--
通讯作者:
Shu X
Shu X
中科院分区:
生物学2区
文献类型:
--
作者:
Lu Y;Rong J;Lai Y;Tao L;Yuan X;Shu X

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免疫组化法检测胃黏膜组织中CD 86、CD 206和HIF-1α的表达。RAW 264.7细胞与H.采用Western blot、PCR和ELISA方法检测不同感染复数(MOI)的pylori细胞中iNOS、CD 86、Arg-1、CD 206和HIF-1α的表达。用荧光探针DCFH-DA检测ROS的表达,用ROS抑制剂NAC或HIF-1α抑制剂YC-1处理巨噬细胞。 免疫组化染色显示,巨噬细胞极化状态与胃粘膜病变的进展和H。幽门感染H. pylori影响巨噬细胞极化,H. pylori可促进巨噬细胞ROS和HIF-1α的表达。低MOI的H. pylori促进M1和M2表型,而高MOI抑制M2表型。此外,ROS抑制减弱HIF-1α表达,并将巨噬细胞极化从M1转换为M2。然而,HIF-1α抑制抑制ROS表达,抑制M1表型和M2表型。ROS或HIF-1α的抑制也抑制了Akt/mTOR通路的激活,这与H.幽门诱导的巨噬细胞极化。 巨噬细胞极化与胃病变的进展和H.幽门感染H. pylori影响巨噬细胞极化状态。ROS和HIF-1α之间的相互作用调节H. pylori通过Akt/mTOR途径诱导的巨噬细胞极化。
The expression of CD86, CD206, and HIF-1α in the gastric mucosa was evaluated through immunohistochemistry. RAW 264.7 cells were cocultured with H. pylori at various multiplicities of infection (MOIs), and iNOS, CD86, Arg-1, CD206, and HIF-1α expression was detected by Western blot, PCR, and ELISA analyses. ROS expression was detected with the fluorescent probe DCFH-DA. Macrophages were also treated with the ROS inhibitor NAC or HIF-1α inhibitor YC-1. Immunohistochemical staining revealed that the macrophage polarization state was associated with the progression of gastric lesions and state of H. pylori infection. The MOI of H. pylori affected macrophage polarization, and H. pylori enhanced the expression of ROS and HIF-1α in macrophages. A low MOI of H. pylori promoted both the M1 and M2 phenotypes, while a high MOI suppressed the M2 phenotype. Furthermore, ROS inhibition attenuated HIF-1α expression and switched macrophage polarization from M1 to M2. However, HIF-1α inhibition suppressed ROS expression and inhibited both the M1 phenotype and the M2 phenotype. Inhibition of ROS or HIF-1α also suppressed the activation of the Akt/mTOR pathway, which was implicated in H. pylori-induced macrophage polarization. Macrophage polarization is associated with the progression of gastric lesions and state of H. pylori infection. The MOI of H. pylori influences the macrophage polarization state. Crosstalk between ROS and HIF-1α regulates H. pylori-induced macrophage polarization via the Akt/mTOR pathway.
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