Department of Basic Medical Sciences, Medical College, Qinghai University, Xining, Qinghai, China.
Research Centre for High Altitude Medicine, Research Centre for High Altitude Medicine, Qinghai University, Xining, Qinghai, China.
Immun Inflamm Dis. 2024 Feb;12(2):e1157. doi: 10.1002/iid3.1157.
Myeloperoxidase (MPO) has been identified as a mediator in various inflammatory diseases. Bacterial infection of the intestine and hypoxia can both lead to inflammatory responses, but the role of MPO in these phenomena remains unclear.
By building the MPO mice, we evaluated relevant inflammatory factors and tissue damage in mice with intestinal Citrobacter rodentium infection and hypoxia. The body weight and excreted microorganisms were monitored. Intestinal tissues were collected 7 days after bacterial infection under hypoxia to undergo haematoxylin-eosin staining and assess the degree of pathological damage. ELISA assays were performed to quantify the serum levels of TNF-α, IFN-γ, IL-6, and IL-1β inflammatory cytokines. PCR, WB, and IF assays were conducted to determine the expression of chemokines MCP1, MIP2, and KC in the colon and spleen.
The C. rodentium infection and hypoxia caused weight loss, intestinal colitis, and splenic inflammatory cells active proliferation in wild-type mice. MPO deficiency alleviated this phenomenon. MPO mice also displayed a significant decline in bacteria clearing ability. The level of TNF-α in the serum and spleen was both lower in MPO hypoxia C. rodentium-infected mice than that in wild-type mice. The chemokines expression levels of MIP2, KC, and MCP1 in the spleen and colon of each bacterial infected group were significantly increased (p < .05), while in hypoxia, the factors in the spleen and colon were decreased (p < .05). MPO deficiency was found to lower the levels of these chemokines compared with wild-type mice.
MPO plays an important role of the inflammatory responses in infectious enteritis and hypoxia in mice, and the loss of MPO may greatly reduce the body's inflammatory responses to fight diseases.
髓过氧化物酶（MPO）已被确定为各种炎症性疾病的介质。肠道细菌感染和缺氧均可导致炎症反应，但 MPO 在这些现象中的作用尚不清楚。
通过构建 MPO 基因敲除小鼠，我们评估了肠道柠檬酸杆菌感染和缺氧小鼠相关炎症因子和组织损伤。监测体重和排出的微生物。在细菌感染后第 7 天，在缺氧条件下采集肠道组织进行苏木精-伊红染色，并评估病理损伤程度。通过酶联免疫吸附试验（ELISA）测定血清中 TNF-α、IFN-γ、IL-6 和 IL-1β 等炎症细胞因子的水平。通过 PCR、WB 和 IF 实验检测结肠和脾脏中趋化因子 MCP1、MIP2 和 KC 的表达。
C. rodentium 感染和缺氧导致野生型小鼠体重减轻、结肠炎和脾脏炎症细胞增殖。MPO 缺乏可减轻这种现象。MPO 基因敲除小鼠的细菌清除能力也显著下降。与野生型小鼠相比，MPO 基因敲除的 C. rodentium 感染缺氧小鼠血清和脾脏中 TNF-α 水平均降低。各细菌感染组的脾脏和结肠中趋化因子 MIP2、KC 和 MCP1 的表达水平均显著升高（p < .05），而在缺氧条件下，这些因子在脾脏和结肠中的表达水平均降低（p < .05）。与野生型小鼠相比，MPO 基因敲除小鼠的这些趋化因子水平降低。
MPO 在小鼠感染性肠炎和缺氧的炎症反应中起重要作用，MPO 的缺失可能会大大降低机体对疾病的炎症反应。
