首页> 外文期刊>Microbial Pathogenesis >Activation of autophagy and IL-10 production are regulated by Jun N-terminal kinase 1 and 2 and p38 mitogen activated protein kinase signaling pathways during Talaromyces marneffei infection within dendritic cells
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Activation of autophagy and IL-10 production are regulated by Jun N-terminal kinase 1 and 2 and p38 mitogen activated protein kinase signaling pathways during Talaromyces marneffei infection within dendritic cells

机译:在树突状细胞内塔拉莫氏菌属Marneffei感染期间,自噬和IL-10产生的激活是由Jun N-末端激酶1和2和P38丝裂原活化蛋白激酶信号传导途径调节

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摘要

Previous study have shown that Talaromyces marneffei (T. marneffei) induced activation of autophagy. Therefore, we explore signaling pathway that regulates activation of autophagy by intracellular signaling mechanisms during T. marneffei infection. Further, we examine c-Jun N-terminal kinase 1 and 2 (JNK1/2) and p38 signaling pathways that regulate IL-1 beta and IL-10 production and activation of autophagy during T. marneffei infection in human dendritic cells (DCs). We found that T. marneffei induced activation of JNK1/2 and p38 in human DCs. Furthermore, the inhibition of JNK1/2 and p38 increased activation of autophagy and decreased the replication of T. marneffei in T. marneffei-infected human DCs. Moreover, IL-1 beta secretion in T. marneffei-infected human DCs was dependent on JNK1/2 and autophagy pathways, whereas IL-10 secretion was dependent on JNK1/2, p38 and autophagy pathways. These data suggest that JNK1/2 and p38 pathways play critical roles in activation of autophagy, the multiplication of T. marneffei and subsequent cytokine production during T. marneffei infection.
机译:以前的研究表明,Talomyces Marneffei(T.Marneffei)诱导自噬激活。因此,我们探讨通过在T.Marneffei感染期间通过细胞内信号传导机制调节自噬激活的信号通路。此外,我们检查C-JUN N-末端激酶1和2(JNK1 / 2)和P38信号传导途径,其调节IL-1β和IL-10在人树突细胞中的T.Marneffei感染期间自噬的生成和激活。我们发现T.Marneffei诱导人类DCS中的JNK1 / 2和P38的激活。此外,JNK1 / 2和P38的抑制增加了自噬激活,并降低了T.Marneffei感染的人类DCS的T.Marneffei的复制。此外,在T.Marneffei感染的人类DC中的IL-1β分泌依赖于JNK1 / 2和自噬途径,而IL-10分泌取决于JNK1 / 2,P38和自噬途径。这些数据表明,JNK1 / 2和P38途径在激活自噬激活时发挥着关键作用,在T.Marneffei感染期间T.Marneffei和随后的细胞因子产生的倍增。

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