Profiling of inflammatory cytokines produced by gingival fibroblasts after human cytomegalovirus infection
Profiling of inflammatory cytokines produced by gingival fibroblasts after human cytomegalovirus infection
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DOI：
10.1111/j.1399-302x.2007.00427.x
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发表时间：
2008-08-01
影响因子：
--
通讯作者：
Parra, B.
中科院分区：
文献类型：
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作者：
Botero, J. E.;Contreras, A.;Parra, B.
简介：本研究的目的是确定牙龈成纤维细胞与人巨细胞病毒（HCMV）体外感染后产生的炎症细胞因子的档案。材料和方法：牙龈成纤维细胞感染Towne株的HCMV和细胞因子的档案中的上清液中进行了研究，使用人类炎症抗体阵列。采用逆转录-聚合酶链反应检测白细胞介素-1 β（IL-1 β）和肿瘤坏死因子-α（TNF-α）的信使RNA（mRNA）表达，并根据HCMV检测结果分析了受感染的牙龈成纤维细胞和牙周炎受试者和非牙周炎受试者的牙龈标本。结果：HCMV感染后牙龈成纤维细胞主要分泌IL-1 α、IL-12 p40、IL-12 p70、IL-6、TNF-α和IL-1 β。HCMV感染后IL-1 β和TNF-α的mRNA表达增加。HCMV阳性牙周炎标本中IL-1 β和TNF-α的产生增加。此外，感染牙龈成纤维细胞产生更多的IL-8，单核细胞趋化蛋白1，巨噬细胞炎症蛋白1 α，1 β随着时间的推移感染后相比，基线。研究的所有细胞因子的最低产量对应于IL-2、IL-4、IL-13和干扰素-γ。减少生产模式观察到粒细胞-巨噬细胞集落刺激因子，IL-7，IL-17，而IL-11和巨噬细胞集落刺激因子增加在72 h postinfection.Conclusions：HCMV感染牙龈成纤维细胞上调促炎相关的细胞因子和趋化因子的生产。在体外和来自患有牙周炎的HCMV阳性受试者的样本中，IL-1 β和TNF-alpha的表达均增加。病毒感染导致的促炎细胞因子和趋化因子的过度产生是HCMV与牙周炎的重要致病机制。
Introduction: The purpose of this study was to determine the profile of inflammatory cytokines that are produced after in vitro infection of gingival fibroblasts with human cytomegalovirus (HCMV).Materials and methods: Gingival fibroblasts were infected with the Towne strain of HCMV and the cytokine profile in the supernatant was studied using a human inflammation antibody array. Expression of messenger RNA (mRNA) using reverse transcription-polymerase chain reaction for interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) was also analyzed in infected gingival fibroblasts and gingival specimens from subjects with and without periodontitis according to HCMV detection. HCMV was determined in subgingival samples by nested polymerase chain reaction.Results: Gingival fibroblasts produced mainly IL-1 alpha, IL-12p40, IL-12p70, IL-6, TNF-alpha, and IL-1 beta after HCMV infection. Expression of mRNA for IL-1 beta and TNF-alpha was increased after HCMV infection. Production of IL-1 beta and TNF-alpha was increased in HCMV-positive periodontitis specimens. In addition, infected gingival fibroblasts produced more IL-8, monocyte chemoattractant protein 1, macrophage inflammatory proteins 1 alpha, and 1 beta over time postinfection in comparison to baseline. The lowest production of all cytokines studied corresponded to IL-2, IL-4, IL-13, and interferon-gamma. A decreasing production pattern was observed for granulocyte-macrophage colony-stimulating factor, IL-7, and IL-17 while IL-11 and macrophage colony-stimulating factor were increased at 72 h postinfection.Conclusions: HCMV infection in gingival fibroblasts upregulated the production of proinflammatory-related cytokines and chemokines. The expression of IL-1 beta and TNF-alpha was increased both in vitro and in specimens from HCMV-positive subjects with periodontitis. The overproduction of proinflammatory cytokines and chemokines as a result of viral infection should be considered an important pathogenic mechanism linking HCMV to periodontitis in vivo.