期刊文献+

TNF-α增强膀胱上皮细胞清除细胞内肺炎克雷伯杆菌

Clearance of intracellular Klebsiella pneumoniae by human urinary epithelial cells enhanced by TNF-α
下载PDF
导出
摘要 目的:研究TNF-α对膀胱上皮细胞内肺炎克雷伯杆菌生存的影响。方法:以肺炎克雷伯杆菌侵入体外培养的人膀胱上皮细胞(T24细胞)为模型,观察在TNF-α等细胞因子处理条件下,不同时间点细胞内细菌数量变化。结果:单独使用TNF-α使T24细胞内的肺炎克雷伯杆菌K5株细菌数量明显减少,联合使用TNF-α与IFN-γ使胞内活菌数量更显著的减少。而IL-1β对细胞内活菌数量无明显影响。过氧化氢酶可以有效抑制TNF-α与IFN-γ刺激的T24细胞抗菌作用,而一氧化氮合酶抑制剂L-NAME无抑制作用。结论:TNF-α能够增强膀胱上皮细胞对抗细胞内肺炎克雷伯杆菌,抗菌机制与细胞产生活性氧(ROS)有关。 Objective: To investigate the effect of proinflammation cytokine TNF-α on the antibacterial activity of urinary epithelial cells against intracellular Klebsiella pneurnoniae. Methods: Monolayers of T24 cells were grown to confluence in 24-well plate. Cells were infected with Klebsiella pneumoniae strain K5, a clinical isolate(approximately 100 bacteria per epithelial cell) for 2 hours. Extracellular bacteria were killed by gentamicin and the cells were incubated with proinflammation cytokines (TNF-α, IFN-γ, IL-1β). After 24 and 48 hours from the initial infection, the cells were lysed with Triton X-100 and viable intracellular bacteria were quantified by plating appropriate dilutions on LB agar plates. Results: In comparison with control, the number of viable intracellular Klebsiella pneumoniae decreased significantly in the cells treated with TNF-α. Combination of TNF-α and IFN-γ further decreased the number of viable intracellular bacteria. On the other hand, IL-1β had no significant effect on the number of viable intracellular Klebsiella pneurrumiae. Antibacterial activity induced by TNF-α and IFN-γ was significantly inhibited by catalase. Conclusion: The clearance of intracellular Klebsiella pneumoniae by human urinary epithelial cells could be enhanced by TNF-α and reactive oxygen species(ROS) were involved in the antibacterial activity.
出处 《四川生理科学杂志》 2013年第1期1-4,共4页 Sichuan Journal of Physiological Sciences
基金 国家自然科学基金(编号:30270688 30570790)
关键词 膀胱上皮细胞 TNF-Α 肺炎克雷伯杆菌 Urinary bladder epithelial cells TNF-α Klebsiella pneumoniae
  • 相关文献

参考文献15

  • 1Finkel T. Oxidant signals and oxidative stress[J]. Curr Opin Cell Biol, 2003, 15(2): 247-254.
  • 2Geiszt M, Leto TL. The Nox family of NAD(P)H oxidases: host defense and beyond[J]. J Biol Chem, 2004, 279(50): 51715- 51718.
  • 3Cox CE, Hinman F Jr. Experiments with induced bacteriuria, vesi- eal emptying and bacterial growth on the mechanism of bladder de- fense to infection[J]. J Uml, 1961, 86(10): 739-748.
  • 4Norden C~, Green GW, Kass EH, et al. Antibacterial mechanisms of urinary blaclder[J]. J Clin Invest, 1968, 47(12): 2689-2700.
  • 5Hand WL, Smith JW, Sanford JP, et al. The antibacterial effect of normal and infected urinary bladder[J]. J Lab Clin Med, 1971, 77 (4): 605-615.
  • 6Harrison G, Cornish J, Vanderwee MA, et al. Host defenee mecha- nisms in the bladder. I. Role of mechanical factors[J]. Br J Exp Pathol, 1988, 69(2): 245-254.
  • 7Deitch EA, Haskel Y, Cruz N, et al. Caco-2 and IEC-18 intestinal epithelial cells exert bactericidal activity through an oxidant-depend- ent pathway[J]. Shock, 1995, 4(5): 345-350.
  • 8Dolapci N, Salo RJ, Cross AS, et al. Antibacterial capacity of oral (epithelial cells from healthy donors and patients with Beheet's dis- ease[J]. Arch Delmatol Res, 2003, 295(3):124-126.
  • 9Schulte-Wissermann H, Mannhardt W, .Schwarz J, etal. Compari- son of the antibacterial effect of uro-epithelial calls from healthy do- nors and children with asymptomatic bacteriuria[J]. Eur J Pediatr, 1985, 144(3): 230-233.
  • 10Sehofer O, Ludwig KH, Mannhardt W, et al. Antibacterial capacity of buecal epithelial cells from healthy donors and children with re- current urinary tract infections[J]. Eur J Pediatr, 1988, 147 (3) : 229-232.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部