Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, 92 APC Road, Calcutta, 700009, West Bengal, India,
Inflammation. 2015 Apr;38(2):812-27. doi: 10.1007/s10753-014-9991-1.
Interaction with the live Staphylococcus aureus promotes secretion of interleukin-8 (IL-8), although the expressions of functional CXCR1 (IL-8RA) in murine macrophages have not been identified. Expression of CXCR1 was induced in S. aureus-infected macrophages, whereas, CXCR1 was undetectable in control macrophages. CXCR1 blocking significantly reduced the phagocytosis of S. aureus and TNF-α, IL-6, IL-1β, IFN-γ, IL-12, and IL-8 production and increased release of MIP-2 and soluble TNF-R1. Increased bacterial catalase and decreased superoxide dismutase (SOD) activities by S. aureus with concomitant decrease in hydrogen peroxide (H2O2), superoxide anion, and nitric oxide (NO) release were observed in case of prior CXCR1 blocking. In the presence of cytochalasin D, S. aureus-mediated induction of IL-8 was inhibited concomitant with decreased bacterial count suggesting that internalization of S. aureus was necessary for induction of IL-8. Shedding of TNF-R1 due to CXCR1 blocking after S. aureus inoculation was critical for neutralization of TNF-α signaling and arrests the inflammation.
与活的金黄色葡萄球菌相互作用会促进白细胞介素-8（IL-8）的分泌，尽管在鼠巨噬细胞中功能性 CXCR1（IL-8RA）的表达尚未确定。金黄色葡萄球菌感染的巨噬细胞中诱导了 CXCR1 的表达，而对照巨噬细胞中则无法检测到 CXCR1。CXCR1 阻断显著减少了金黄色葡萄球菌的吞噬作用以及 TNF-α、IL-6、IL-1β、IFN-γ、IL-12 和 IL-8 的产生，并增加了 MIP-2 和可溶性 TNF-R1 的释放。在金黄色葡萄球菌预先阻断 CXCR1 的情况下，观察到金黄色葡萄球菌的细菌过氧化氢酶增加和超氧化物歧化酶（SOD）活性降低，同时伴随着过氧化氢（H2O2）、超氧阴离子和一氧化氮（NO）的释放减少。在细胞松弛素 D 的存在下，金黄色葡萄球菌介导的 IL-8 诱导被抑制，同时细菌数量减少，表明金黄色葡萄球菌的内化对于 IL-8 的诱导是必要的。金黄色葡萄球菌接种后由于 CXCR1 阻断而导致的 TNF-R1 脱落对于中和 TNF-α信号和阻止炎症至关重要。
