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Cytokines and Mycobacterium leprae induce apoptosis in human Schwann cells.

机译:细胞因子和麻风分枝杆菌诱导人雪旺细胞凋亡。

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The development of deformities during the course of leprosy disease is a major public health concern worldwide. It is possible that cytokine production and apoptosis of Schwann cells (SCs) directly affect nerve degeneration and regeneration leading to injury of the myelin sheath and axon. In the present study, the expression of TNFalpha, TGFbeta, and their receptors, in addition to cell death triggered by cytokines or whole Mycobacterium leprae were investigated in a human SC line. The results showed the presence of TNF-Rs and TGF-RII on the SC membrane and the shedding of TNF-Rs during the culture period. Evaluation of cell death was performed through TUNEL and flow cytometry techniques. TNFalpha/TGFbeta combination as well as M. leprae infection triggered an increase in the apoptosis rate in the cultured SC. Moreover, reverse transcriptase-polymerase chain reaction assay revealed that M. leprae upregulated the expression of such cytokines and their receptors on the SC line. Despite the detection of TNFalpha mRNA, no protein was found in the culture supernatants. The data indicate that induction of SC death after cell interaction with M. leprae may, in fact, be implicated in the pathogenesis of nerve damage, which can most likely be modulated by in vivo cytokine production.
机译:麻风病期间畸形的发展是全世界主要的公共卫生问题。雪旺细胞(SCs)的细胞因子产生和凋亡可能直接影响神经变性和再生,从而导致髓鞘和轴突损伤。在本研究中,在人SC系中研究了TNFalpha,TGFbeta及其受体的表达,以及由细胞因子或整个麻风分支杆菌引发的细胞死亡。结果显示在培养期间,SC膜上存在TNF-Rs和TGF-RII,并且TNF-Rs脱落。通过TUNEL和流式细胞术技术评估细胞死亡。 TNFalpha / TGFbeta组合以及麻风分枝杆菌感染触发了培养的SC细胞凋亡率的增加。此外,逆转录酶-聚合酶链反应分析表明,麻风分枝杆菌上调了这种细胞因子及其受体在SC系上的表达。尽管检测到TNFalpha mRNA,但在培养上清液中未发现蛋白质。数据表明,与麻风分枝杆菌相互作用后,SC死亡的诱导可能与神经损伤的发病机制有关,神经损伤的发生机制很可能由体内细胞因子的产生来调节。

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