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首页> 外文期刊>Infection and immunity >Streptococcal Histone Induces Murine Macrophages To Produce Interleukin-1 and Tumor Necrosis Factor Alpha
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Streptococcal Histone Induces Murine Macrophages To Produce Interleukin-1 and Tumor Necrosis Factor Alpha

机译：链球菌组蛋白诱导小鼠巨噬细胞产生白介素-1和肿瘤坏死因子α。

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The histone-like protein (HlpA) is highly conserved among streptococci. After lysis of streptococci in infected tissues, HlpA can enter the bloodstream and bind to proteoglycans in the glomerular capillaries of kidneys, where it can react with antibodies or stimulate host cell receptors. Deposits of streptococcal antigens in tissues have been associated with localized acute inflammation. In this study, we measured the ability of purified HlpA (5 to 100 μg/ml), fromStreptococcus mitis, to induce the production of proinflammatory cytokines by cultured, murine peritoneal macrophages. The release of tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1) was time and concentration dependent and was not diminished by the presence of polymyxin B. Exposure of macrophages to a mixture of HlpA and lipoteichoic acid resulted in a synergistic response in the production of both TNF-α and IL-1. Stimulation with a mixture of HlpA and heparin resulted in reduced cytokine production (50% less IL-1 and 76% less TNF-α) compared to that by cells incubated with HlpA alone. The inclusion of antibodies specific to HlpA in macrophage cultures during stimulation with HlpA did not affect the quantity of TNF-α or IL-1 produced. These observations suggest that streptococcal histone may contribute to tissue injury at infection sites by promoting monocytes/macrophages to synthesize and release cytokines that initiate and exacerbate inflammation. Streptococcus pyogenes, which can infect tissues in enormous numbers, may release sufficient amounts of HlpA to reach the kidneys and cause acute poststreptococcal glomerulonephritis.
机译：组蛋白样蛋白（HlpA）在链球菌中高度保守。链球菌在感染组织中溶解后，HlpA可以进入血液并与肾脏的肾小球毛细血管中的蛋白聚糖结合，在这里它可以与抗体反应或刺激宿主细胞受体。链球菌抗原在组织中的沉积与局部急性炎症有关。在这项研究中，我们测量了来自链球菌的纯化HlpA（5至100μg/ ml）诱导培养的鼠腹膜巨噬细胞诱导促炎细胞因子产生的能力。肿瘤坏死因子α（TNF-α）和白细胞介素1（IL-1）的释放是时间和浓度依赖性的，并且不会因多粘菌素B的存在而减少。巨噬细胞暴露于HlpA和脂磷壁酸的混合物导致TNF-α和IL-1产生的协同反应。与仅与HlpA孵育的细胞相比，用HlpA和肝素的混合物刺激导致细胞因子生成减少（IL-1减少50％，TNF-α减少76％）。在HlpA刺激过程中，巨噬细胞培养物中对HlpA特异的抗体的加入不会影响所产生的TNF-α或IL-1的数量。这些观察结果表明，链球菌组蛋白可能通过促进单核细胞/巨噬细胞合成并释放引发和加剧炎症的细胞因子而导致感染部位的组织损伤。化脓性链球菌可大量感染组织，可释放足够量的HlpA到达肾脏并引起急性链球菌性肾小球肾炎。

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