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首页> 外文期刊>Microbial Pathogenesis >Mycoplasma pneumoniae subtype-independent induction of proinflammatory cytokines in THP-1 cells
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Mycoplasma pneumoniae subtype-independent induction of proinflammatory cytokines in THP-1 cells

机译：THP-1细胞中肺炎支原体亚型非依赖性促炎细胞因子的诱导

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摘要

Mycoplasma pneumoniae can be divided into two main subtypes depending on the amino acid sequences of the P1 adhesin and the P65 protein, both located in the attachment organelle. Differences between these subtypes in infectivity, virulence and interaction with host cells have not been extensively studied. Using ELISA to measure released protein and real-time PCR to quantify mRNA, we have demonstrated that both M. pneumoniae subtypes significantly increased tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8) at comparable levels in THP-1 cells over a 72 h period of time. However, subtype 2 induced a statistically significant increase (P<0.001) in the release of interleukin-1beta at 24 h post-infection compared to subtype 1. These data provide evidence that the induction of proinflammatory cytokine gene and protein expression by M. pneumoniae is not dependent on the infecting subtype.
机译：肺炎支原体可以分为两个主要的亚型，这取决于位于粘附细胞器中的P1粘附素和P65蛋白的氨基酸序列。这些亚型之间在感染性，毒力和与宿主细胞相互作用方面的差异尚未得到广泛研究。使用ELISA来测量释放的蛋白质并通过实时PCR定量mRNA，我们已经证明肺炎支原体亚型都显着增加了肿瘤坏死因子-α（TNF-alpha），白介素6（IL-6）和白介素8（在72小时内，THP-1细胞中的IL-8水平处于可比水平。然而，与亚型1相比，亚型2在感染后24 h诱导了白细胞介素1β释放的统计学显着增加（P <0.001）。这些数据提供了证据，表明肺炎支原体可诱导促炎性细胞因子基因和蛋白质表达。不依赖于感染亚型。

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