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首页> 外文期刊>BMC Immunology >Streptococcus pneumoniae stabilizes tumor necrosis factor α mRNA through a pathway dependent on p38 MAPK but independent of Toll-like receptors
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Streptococcus pneumoniae stabilizes tumor necrosis factor α mRNA through a pathway dependent on p38 MAPK but independent of Toll-like receptors

机译：肺炎链球菌通过依赖于p38 MAPK但不依赖Toll样受体的途径稳定肿瘤坏死因子αmRNA

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Background Streptococcus pneumoniae is a human pathogenic bacteria and a major cause of severe invasive diseases, including pneumonia, bacteremia, and meningitis. Infections with S. pneumoniae evoke a strong inflammatory response, which plays a major role in the pathogenesis of pneumococcal disease. Results In this study, we have examined how S. pneumoniae affects expression of the inflammatory cytokine tumor necrosis factor (TNF) α, and the molecular mechanisms involved. Secretion of TNF-α was strongly induced by S. pneumoniae, which was able to stabilize TNF-α mRNA through a mechanism dependent on the viability of the bacteria as well as the adenylate uridylate-rich elements in the 3'untranslated region of TNF-α mRNA. The ability of S. pneumoniae to stabilize TNF-α mRNA was dependent on the mitogen-activated protein kinase (MAPK) p38 whereas inhibition of Toll-like receptor signaling via MyD88 did not affect S. pneumoniae-induced mRNA stabilization. P38 was activated through a pathway involving the upstream kinase transforming growth factor-activated kinase 1 and MAPK kinase 3. Conclusion Thus, S. pneumoniae stabilizes TNF-α mRNA through a pathway dependent on p38 but independent of Toll-like receptors. Production of TNF-α may contribute significantly to the inflammatory response raised during pneumococcal infection.
机译：背景技术肺炎链球菌是一种人类致病细菌，是包括肺炎，菌血症和脑膜炎在内的严重侵袭性疾病的主要原因。肺炎链球菌感染引起强烈的炎症反应，这在肺炎球菌疾病的发病机理中起主要作用。结果在这项研究中，我们研究了肺炎链球菌如何影响炎性细胞因子肿瘤坏死因子（TNF）α的表达及其涉及的分子机制。肺炎链球菌强烈诱导TNF-α的分泌，它能够通过依赖于细菌和TNF-α3'非翻译区中富含腺苷酸尿苷酸元素的生存力的机制稳定TNF-αmRNA。 αmRNA。肺炎链球菌稳定TNF-αmRNA的能力取决于有丝分裂原激活的蛋白激酶（MAPK）p38，而通过MyD88抑制Toll样受体信号转导不会影响肺炎链球菌诱导的mRNA稳定。通过涉及上游激酶转化生长因子激活的激酶1和MAPK激酶3的途径激活P38。结论因此，肺炎链球菌通过依赖于p38但独立于Toll样受体的途径稳定TNF-αmRNA。 TNF-α的产生可能对肺炎球菌感染过程中引起的炎症反应有重要贡献。

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