Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression.
Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression.
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DOI：
10.1111/j.1399-302x.2009.00538.x
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发表时间：
2009-12
影响因子：
--
通讯作者：
Gibson FC 3rd
中科院分区：
文献类型：
--
作者：
Baer MT;Huang N;Gibson FC 3rd
牙龈卟啉单胞菌是一种与广泛侵袭性牙周病密切相关的牙周致病菌。模式识别受体（PRRs）参与宿主对该生物体的反应。可能先前未被识别为宿主对牙龈卟啉单胞菌应答的一部分的PRR也参与宿主对该生物体的应答。采用qRT-PCR，我们观察到在用牙龈卟啉单胞菌菌株381培养2、6和24小时时msr 1基因表达增加。流式细胞术显示到24小时时间点SR-A蛋白的表面表达增加。用附着受损的牙龈卟啉单胞菌fimA突变体（DPG 3）培养的巨噬细胞表达中等水平的SR-A表达。热灭活的牙龈卟啉单胞菌刺激类似于活细菌的SR-A表达，并且纯化的牙龈卟啉单胞菌荚膜多糖刺激巨噬细胞SR-A表达，表明活的完整生物体对于巨噬细胞应答中的SR-A蛋白表达不是必需的。由于已知SR-A在巨噬细胞的脂质摄取中起作用，我们测试了低密度脂蛋白（LDL）影响巨噬细胞对牙龈卟啉单胞菌的SR-A反应的能力，并且观察到LDL对牙龈卟啉单胞菌引起的SR-A表达没有影响。最后，我们观察到SR-A敲除（SR-A−/−）小鼠巨噬细胞产生的肿瘤坏死因子（TNF）-α显著高于与牙龈卟啉单胞菌培养的野生型小鼠巨噬细胞。这些数据表明，巨噬细胞在对牙龈卟啉单胞菌的反应中表达SR-A，并支持该分子在巨噬细胞产生TNF-α至该生物体中发挥作用。
Porphyromonas gingivalis is a periodontopathic bacterium closely associated with generalized aggressive periodontal disease. Pattern recognition receptors (PRRs) participate in host response to this organism. It is likely that PRRs not previously recognized as part of the host response to P. gingivalis also participate in host response to this organism. Employing qRT-PCR, we observed increased msr1 gene expression at 2, 6, and 24h of culture with P. gingivalis strain 381. Flow cytometry revealed increased surface expression of SR-A protein by the 24h time point. Macrophages cultured with an attachment impaired P. gingivalis fimA- mutant (DPG3) expressed intermediate levels of SR-A expression. Heat-killed P. gingivalis stimulated SR-A expression similar to live bacteria, and purified P. gingivalis capsular polysaccharide stimulated macrophage SR-A expression, indicating that live whole organisms are not necessary for SR-A protein expression in macrophage response. As SR-A is known to play a role in lipid uptake by macrophages, we tested the ability of low-density lipoprotein (LDL) to influence the SR-A response of macrophages to P. gingivalis, and observed no effect of LDL on P. gingivalis-elicited SR-A expression. Lastly, we observed that SR-A knockout (SR-A−/−) mouse macrophages produced significantly more tumor necrosis factor (TNF)-α than wild type mouse macrophages cultured with P. gingivalis. These data identify that SR-A is expressed by macrophages in response to P. gingivalis, and support that this molecule plays a role in TNF-α production by macrophages to this organism.