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首页> 外文期刊>American Journal of Physiology >Mycoplasma fermentans and TNF-beta interact to amplify immune-modulating cytokines in human lung fibroblasts.
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Mycoplasma fermentans and TNF-beta interact to amplify immune-modulating cytokines in human lung fibroblasts.

机译：发酵支原体和TNF-β相互作用，以放大人肺成纤维细胞中的免疫调节细胞因子。

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摘要

Mycoplasma can establish latent infections and are associated with arthritis, leukemia, and chronic lung disease. We developed an experimental model in which lung cells are deliberately infected with Mycoplasma fermentans. Human lung fibroblasts (HLF) were exposed to live M. fermentans and immune-modulating cytokine release was assessed with and without known inducers of cytokine production. M. fermentans increased IL-6, IL-8/CXCL8, MCP-1/CCL2, and Gro-alpha/CXCL1 production. M. fermentans interacted with TNF-beta to release more IL-6, CXCL8, and CXCL1 than predicted by the responses to either stimulus alone. The effects of live infection were recapitulated by exposure to M. fermentans-derived macrophage-activating lipopeptide-2 (MALP-2), a Toll-like receptor-2- and receptor-6-specific ligand. The synergistic effect of combined stimuli was more pronounced with prolonged incubations. Preexposure to TNF-beta sensitized the cells to subsequent MALP-2 challenge, but preexposure to MALP-2 did not alter the IL-6 response to TNF-beta. Exposure to M. fermentans or MALP-2 did not enhance nuclear localization, DNA binding, or transcriptional activity of NF-kappaB and did not modulate early NF-kappaB activation in response to TNF-beta. Application of specific inhibitors of various MAPKs suggested that p38 and JNK/stress-activated protein kinase were involved in early IL-6 release after exposure to TNF-beta and M. fermentans, respectively. The combined response to M. fermentans and TNF-beta, however, was uniquely sensitive to delayed application of SP-600125, suggesting that JNK/stress-activated protein kinase contributes to the amplification of IL-6 release. Thus M. fermentans interacts with stimuli such as TNF-beta to amplify lung cell production of immune-modulating cytokines. The mechanisms accounting for this interaction can now be dissected with the use of this in vitro model.
机译：支原体可以建立潜在的感染，并与关节炎，白血病和慢性肺病相关。我们开发了一个实验模型，其中肺细胞被发酵支原体故意感染。将人肺成纤维细胞（HLF）暴露于活的发酵乳杆菌，并在有或没有已知细胞因子生成诱导剂的情况下评估免疫调节细胞因子的释放。发酵发酵单胞菌增加了IL-6，IL-8 / CXCL8，MCP-1 / CCL2和Gro-alpha / CXCL1的产量。发酵单胞菌与TNF-β相互作用释放的IL-6，CXCL8和CXCL1比单独对任一刺激的反应预期的要多。通过暴露于发酵发酵单胞菌衍生的巨噬细胞激活脂肽2（MALP-2），Toll样受体2和受体6特异性配体来概括活感染的影响。随着时间的延长，联合刺激的协同作用更加明显。预先暴露于TNF-β使细胞对随后的MALP-2攻击敏感，但预先暴露于MALP-2不会改变IL-6对TNF-beta的反应。暴露于发酵酵母或MALP-2不会增强核定位，DNA结合或NF-κB的转录活性，也不会调节对TNF-β的早期NF-κB活化。各种MAPK的特异性抑制剂的应用表明，p38和JNK /应激激活的蛋白激酶分别与TNF-β和发酵乳杆菌接触后，参与IL-6的早期释放。然而，对发酵乳杆菌和TNF-β的联合反应对SP-600125的延迟应用具有独特的敏感性，这表明JNK /应激激活的蛋白激酶有助于IL-6释放的放大。因此，发酵发酵单胞菌与刺激物如TNF-β相互作用，以放大肺细胞产生的免疫调节细胞因子。现在，可以使用此体外模型来分析解释这种相互作用的机制。

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