Induction of CC chemokines in human peripheral blood mononuclear cells by staphylococcal exotoxins and its prevention by pentoxifylline
Induction of CC chemokines in human peripheral blood mononuclear cells by staphylococcal exotoxins and its prevention by pentoxifylline
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DOI：
10.1002/jlb.66.1.158
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发表时间：
1999-07-01
影响因子：
5.5
通讯作者：
Krakauer, T
中科院分区：
文献类型：
--
作者：
Krakauer, T
我们研究了可能与金黄色葡萄球菌（细菌性关节炎的主要病原体）的关节源性活动相关的炎症过程。用葡萄球菌中毒性休克综合征毒素-1（TSST-1）或肠毒素B（SE B）刺激人外周血单个核细胞（PBMC），检测趋化因子的产生。TSST-1和SEE均诱导高水平（ng/mL）的MIP-1 α、MIP-1 β和MCP-1。这些趋化因子的诱导主要通过用葡萄球菌外毒素（SE）直接刺激PBMC而发生，而不需要IL-1和TNF-α的干预。SE诱导的趋化因子的产生被抗DR和抗CD 2抗体部分阻断。细胞分离揭示单核细胞作为这些趋化因子的细胞来源，然而，加入纯化的T细胞扩增了产生的趋化因子的水平，表明结合在抗原呈递细胞上的SE与T细胞的同源相互作用也有助于趋化因子的产生。这些趋化因子对白细胞的激活和募集可能通过组织损伤和T淋巴细胞的募集，也可能引发自身免疫反应，从而促进葡萄球菌引起的人类脓毒性关节炎的病理生理学。抗炎剂喷替福林完全抑制了这些趋化因子的产生。
We investigated the inflammatory processes that might be associated with the arthrogenic activity of Staphylococcus aureus, the principal causative agent of bacterial arthritis. Human peripheral blood mononuclear cells (PBMC) were stimulated with the staphylococcal toxic shock, syndrome toxin-1 (TSST-1) or enterotoxin B (SEB) and the production of chemokines tvas examined. Both TSST-1 and SEE induced high levels (ng/mL) of MIP-1 alpha, MIP-1 beta, and MCP-1, The induction of these chemokines occurred mostly by direct stimulation of PBMC with staphylococcal exotoxins (SE), without requiring the intervention of IL-1 and TNF-alpha. The production of SE-induced chemokines was blocked partially by anti-DR and anti-CD2 antibodies. Cell separation revealed monocytes as the cell source of these chemokines, However, addition of purified T cells amplified the levels of chemokine produced, suggesting that cognate interaction of SE bound on antigen-presenting cells with T cells also contributes to chemokine production. The activation and recruitment of leukocytes by these chemokines may contribute to the pathophysiology of septic arthritis caused by staphylococci in humans through tissue injury and the recruitment of T lymphocytes, perhaps also initiating autoimmune responses. Pentoxifylline, an anti-inflammatory agent, completely inhibited the production of these chemokines.