Human cytomegalovirus and Epstein-Barr virus inhibit oral bacteria-induced macrophage activation and phagocytosis.

Human cytomegalovirus and Epstein-Barr virus inhibit oral bacteria-induced macrophage activation and phagocytosis.
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人类巨细胞病毒和爱泼斯坦 - 巴尔病毒抑制口腔细菌诱导的巨噬细胞激活和吞噬作用。

DOI:
10.1111/j.1399-302x.2009.00504.x
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发表时间:
2009-06
影响因子:
--
通讯作者:
Li M
Li M
中科院分区:
其他
文献类型:
--
作者:
Lin YL;Li M

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牙周病是一种由牙周微生物引起的炎症性疾病。病毒如人巨细胞病毒(HCMV)和EB病毒(EBV)与某些类型的牙周病有关,但它们在促进疾病中的作用尚不清楚。由于这两种病毒感染人类巨噬细胞,这些细胞在清除病原菌中起关键作用,因此病毒可能通过抑制巨噬细胞对入侵病原体的防御机制来改变巨噬细胞的功能能力。用选定的口腔细菌刺激后,评价了HCMV或EBV预感染的巨噬细胞。通过测量培养基中产生的肿瘤坏死因子-α(TNF-α)水平来测定细菌诱导的巨噬细胞活化,并通过异硫氰酸荧光素标记细菌的吞噬试验来分析吞噬活性。病毒感染的巨噬细胞也进行了半定量聚合酶链反应,以测量Toll样受体9的表达,这是参与吞噬相关途径的激活。HCMV和EBV均能显著抑制口腔细菌诱导的TNF-α产生,抑制巨噬细胞的吞噬活性,下调Toll样受体9的表达。HCMV或EBV感染抑制了巨噬细胞对细菌攻击的功能性反应,从而表明它们在牙周病发展中的致病作用。
Periodontal disease is an inflammatory condition caused by periodontal microorganisms. Viruses such as human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) are associated with certain types of periodontal disease, but their roles in promoting the disease are unclear. Because both viruses infect human macrophages, cells which play key roles in the clearance of pathogenic bacteria, it is likely that the viruses alter the functional capacity of macrophages by inhibiting their defense mechanisms against invading pathogens. Macrophages preinfected with HCMV or EBV were evaluated following stimulation by selected oral bacteria. Bacteria-induced macrophage activation was assayed by measuring the levels of tumor necrosis factor-α (TNF-α) produced in the media, and phagocytic activity was analysed by a phagocytosis assay with fluorescein isothiocyanate-labeled bacteria. The virus-infected macrophages were also subjected to semi-quantitative polymerase chain reaction to measure the expression of toll-like receptor 9, which is involved in the activation of phagocytosis-related pathways. Both HCMV and EBV significantly diminished the TNF-α production typically induced by oral bacteria, inhibited the phagocytic activity of macrophages, and downregulated the expression of toll-like receptor 9. Infection by HCMV or EBV inhibits the functional ability of macrophages to respond to bacterial challenge, thereby suggesting their pathogenic role in the development of periodontal disease.