Department of Physiology, Immunology Laboratory, University of Calcutta, 92 A.P.C. Road, Calcutta 700009, West Bengal, India.
Department of Physiology, Immunology Laboratory, University of Calcutta, 92 A.P.C. Road, Calcutta 700009, West Bengal, India.
Microb Pathog. 2017 Dec;113:460-471. doi: 10.1016/j.micpath.2017.11.028. Epub 2017 Nov 21.
Currently, very few studies are available on the expression of CXCR1 in mouse macrophages having both intact TNFR1 and IL-1R or their deficiency in relation to acute S. aureus infection. Peritoneal macrophages from mice neutralized singly for TNFR1or IL-1R, or for both TNFR1 and IL-1R were infected with S. aureus in vitro and their ability to secrete cytokines and reactive oxygen species (ROS) were determined. It was observed that the release of TNF-α and IL-1β in response to S. aureus infection was decreased in macrophages when both TNFR1 and IL-1R were neutralized. The amount of HO, superoxide anion, nitric oxide release and bacterial CFU were significantly decreased in TNFR1 plus IL-1R blocked macrophages when compared with macrophages having intact receptors at 60 min of S. aureus infection. There was decrement of CXCL8 (IL-8) release and expression of CXCR1 in macrophages during dual receptor (TNFR1 plus IL-1R) blocking prior to stimulation with S. aureus. Expression of CXCR1 on murine peritoneal macrophages was evaluated by immunoblots from lysate at 60 min after S. aureus infection. It was observed that at 60 min after S. aureus infection in murine peritoneal macrophages, the expression of CXCR1 was increased significantly (p < 0.05) in comparison to the control groups. CXCR1 expression was decreased significantly (p < 0.05) in macrophages pre-incubated separately with anti-TNFR1 antibody (10 μg/ml) or IL-1R antagonist protein (240 ng/ml) at 60 min after S. aureus infection. However, blocking of both TNFR1 as well as IL-1R in macrophages downregulated the CXCR1expression in comparison to the groups either pre-incubated with anti-TNFR1 antibody or IRAP alone.
目前，关于在完整的 TNFR1 和 IL-1R 或其缺陷的情况下，CXCR1 在具有完整 TNFR1 和 IL-1R 或其缺陷的小鼠巨噬细胞中的表达，只有极少数研究。将单独中和 TNFR1 或 IL-1R 或同时中和 TNFR1 和 IL-1R 的小鼠腹腔巨噬细胞在体外感染金黄色葡萄球菌，并测定其分泌细胞因子和活性氧 (ROS) 的能力。结果观察到，当同时中和 TNFR1 和 IL-1R 时，金黄色葡萄球菌感染后 TNF-α和 IL-1β的释放减少。与具有完整受体的巨噬细胞相比，在金黄色葡萄球菌感染 60 分钟时，TNFR1 加 IL-1R 阻断的巨噬细胞中 HO、超氧阴离子、一氧化氮释放和细菌 CFU 的数量显着减少。在金黄色葡萄球菌刺激之前，双重受体 (TNFR1 加 IL-1R) 阻断期间，CXCL8 (IL-8) 的释放和 CXCR1 的表达在巨噬细胞中减少。用金黄色葡萄球菌感染后 60 分钟的裂解物通过免疫印迹评估鼠腹膜巨噬细胞上的 CXCR1 表达。结果观察到，在金黄色葡萄球菌感染后 60 分钟，与对照组相比，鼠腹膜巨噬细胞中 CXCR1 的表达显着增加 (p<0.05)。在金黄色葡萄球菌感染后 60 分钟，分别用抗 TNFR1 抗体 (10 μg/ml) 或 IL-1R 拮抗剂蛋白 (240 ng/ml) 预孵育的巨噬细胞中，CXCR1 表达显着降低 (p<0.05)。然而，与单独用抗 TNFR1 抗体或 IRAP 预孵育的组相比，巨噬细胞中同时阻断 TNFR1 和 IL-1R 下调了 CXCR1 的表达。
