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Mycoplasma fermentans inhibits tumor necrosis factor alpha-induced apoptosis in the human myelomonocytic U937 cell line.

机译:发酵支原体抑制人骨髓单核细胞U937细胞系中肿瘤坏死因子α诱导的凋亡。

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Mycoplasma fermentans (M. fermentans) was shown to be involved in the alteration of several eukaryotic cell functions (i.e. cytokine production, gene expression), and was suggested as a causative agent in arthritic diseases involving impaired apoptosis. We investigated whether M. fermentans has a pathogenic potential by affecting tumor necrosis factor (TNF)alpha-induced apoptosis in the human myelomonocytic U937 cell line. A significant reduction in the TNFalpha-induced apoptosis (approximately 60%) was demonstrated upon either infection with live M. fermentans or by stimulation with non-live M. fermentans. To investigate the mechanism of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane potential (DeltaPsim) and the protease activity of caspase-8 were measured. In the infected cells, the reduction of DeltaPsim was inhibited (approximately 75%), and an approximately 60% reduction of caspase-8 activity was measured. In conclusion, M. fermentans significantly inhibits TNFalpha-induced apoptosis in U937 cells, and its effect is upstream of the mitochondria and upstream of caspase-8.
机译:发酵支原体(M. fermentans)被证明参与几种真核细胞功能的改变(即细胞因子的产生,基因表达),并被认为是引起细胞凋亡的关节炎疾病的病原体。我们通过影响人类骨髓单核细胞U937细胞系中的肿瘤坏死因子(TNF)α诱导的细胞凋亡,研究了发酵发酵单胞菌是否具有致病性。在用活发酵支原体感染或用非活发酵支原体刺激后,证明TNFα诱导的凋亡显着减少(约60%)。为了研究发酵发酵单胞菌抗凋亡作用的机制,测定了线粒体跨膜电位(DeltaPsim)的降低和caspase-8的蛋白酶活性。在被感染的细胞中,DeltaPsim的降低被抑制(大约75%),并且caspase-8活性降低了大约60%。总之,发酵发酵单胞菌显着抑制U937细胞中TNFalpha诱导的凋亡,其作用是在线粒体上游和caspase-8上游。

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