Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006 Jiangxi Province, China.
Department of Gastroenterology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006 Jiangxi Province, China.
Oxid Med Cell Longev. 2020 Dec 8;2020:5281795. doi: 10.1155/2020/5281795. eCollection 2020.
The expression of CD86, CD206, and HIF-1 in the gastric mucosa was evaluated through immunohistochemistry. RAW 264.7 cells were cocultured with at various multiplicities of infection (MOIs), and iNOS, CD86, Arg-1, CD206, and HIF-1 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-1 inhibitor YC-1.
Immunohistochemical staining revealed that the macrophage polarization state was associated with the progression of gastric lesions and state of infection. The MOI of affected macrophage polarization, and enhanced the expression of ROS and HIF-1 in macrophages. A low MOI of promoted both the M1 and M2 phenotypes, while a high MOI suppressed the M2 phenotype. Furthermore, ROS inhibition attenuated HIF-1 expression and switched macrophage polarization from M1 to M2. However, HIF-1 inhibition suppressed ROS expression and inhibited both the M1 phenotype and the M2 phenotype. Inhibition of ROS or HIF-1 also suppressed the activation of the Akt/mTOR pathway, which was implicated in -induced macrophage polarization.
Macrophage polarization is associated with the progression of gastric lesions and state of infection. The MOI of influences the macrophage polarization state. Crosstalk between ROS and HIF-1 regulates -induced macrophage polarization via the Akt/mTOR pathway.
通过免疫组织化学评估胃黏膜中 CD86、CD206 和 HIF-1 的表达。用不同感染复数（MOI）的与 RAW 264.7 细胞共培养，并通过 Western blot、PCR 和 ELISA 分析检测 iNOS、CD86、Arg-1、CD206 和 HIF-1 的表达。用荧光探针 DCFH-DA 检测 ROS 表达。还用 ROS 抑制剂 NAC 或 HIF-1 抑制剂 YC-1 处理巨噬细胞。
免疫组织化学染色表明，巨噬细胞极化状态与胃病变进展和感染状态有关。MOI 影响巨噬细胞极化，增强巨噬细胞中 ROS 和 HIF-1 的表达。低 MOI 的促进 M1 和 M2 表型，而高 MOI 抑制 M2 表型。此外，ROS 抑制减弱 HIF-1 表达并将巨噬细胞极化从 M1 转换为 M2。然而，HIF-1 抑制抑制 ROS 表达并抑制 M1 表型和 M2 表型。ROS 或 HIF-1 的抑制也抑制 Akt/mTOR 通路的激活，该通路参与了诱导的巨噬细胞极化。
巨噬细胞极化与胃病变进展和感染状态有关。MOI 影响巨噬细胞极化状态。ROS 和 HIF-1 之间的串扰通过 Akt/mTOR 通路调节诱导的巨噬细胞极化。
