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MIF、TNF-α在肺结核组织中表达和意义的初步探讨 被引量:11

The expression and its significance of MIF、TNF-α in pulmonary tuberculosis tissue
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摘要 目的检测MIF、TNF-α在肺结核组织中和正常肺组织中表达的差异,以及2者之间的关系,探讨MIF、TNF-α在肺结核中所起的作用和价值。方法正常肺组17例,肺结核组33例。肺结核组中的样本分类概括为空洞组18例(包含18例结节组和18例结旁组)和无空洞组15例(包含15例结节组和15例结旁组)。用免疫组化技术检测肺标本中蛋白MIF、TNF-α的表达。结果 MIF、TNF-α在肺结核结节中大部分为类上皮和朗汉斯巨细胞表达,其表达明显高于结节旁,结节旁明显高于正常肺组织;且空洞组表达均高于无空洞组。在肺结核结节中MIF和TNF-α呈正相关。结论肺结核患者结核结节中存在MIF、TNF-α的高表达,且2者呈明显正相关。说明MIF、TNF-α与肺结核结节的形成密切相关,MIF与TNF-α在肺结核结节中可能互相诱导、刺激,共同放大炎性反应;且MIF、TNF-α产生过多可能与肺结核空洞的形成有关。 Objective To study the expression difference and clinical value of MIF,TNF-α in pulmonary tuberculosis(PTB) tissue and normal lung tissue.Methods The lung specimens were divided into normal control group(17 cases) and PTB group(33 cases).All the specimens in PTB group were divided into 15 non-cavity groups(including 15 tubercle tissues and 15 peripheral tissues of tubercle) and 18 cavity groups(including 18 tubercle tissues and 18 peripheral tissues of tubercle).The expressions of MIF、TNF-α in lung tussues were examined with quantitative immunohistochemistry assay.Results There are a lot of expressions of MIF、TNF-α,in which most of them were expressed by epithelioid cell and Langhans' giant cells in tubercles of PTB.The expression levels of MIF、TNF-α in the tubercles of PTB is much higher than that in the peripheral tissues of the tubercles in PTB,which was much higher than that in the normal lungs.The expression levels of MIF、TNF-α of cavity groups is higher than that of non-cavity groups.The tubercles of PTB,MIF and TNF-α are positively correlated.Conclusions MIF、TNF-α are closely correlated with the formation of tubercles in PTB.The overexpression of MIF and TNF-α in the tubercles of PTB might play a crucial role in the formation of cavity of PTB.
出处 《中国防痨杂志》 CAS 2011年第3期153-157,I0001,共6页 Chinese Journal of Antituberculosis
关键词 结核 巨噬细胞游走抑制因子 肿瘤坏死因子-Α tuberculosis pulmonary macrophage migration inhibitory factor tumor necrosis factor-alpha
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  • 1唐神结,肖和平.细胞凋亡与结核病[J].中华结核和呼吸杂志,2004,27(7):477-480. 被引量:9
  • 2中华医学会.急性肺损伤和急性呼吸窘迫综合征的诊断标准(草案)[J].中华结核和呼吸杂志,2000,23(4):203-203.
  • 3陆德源.医用微生物学,第3版[M].北京:人民卫生出版社,1989.175-176.
  • 4Bacher, M., Metz, C.N., Calandra, T., Mayer, K., Chesney, J., Lohoff, M., Gemsa, D., Donnelly, T., and Bucala, R. (1996). An essential regulatory role for macrophage migration inhibitory factor in T-cell activation. Proc. Natl. Acad. Sci. USA 93: 7849-7854.
  • 5Barton, A., Lamb, R., Symmons, D., Silman, A., Thomson, W., Worthingtonl, J., and Donn, R. (2003). Macrophage migration inhibitory factor (M/F) gene polymorphism is associated with susceptibility to but not severity of inflammatory polyarthritis. Genes Immun. 4: 487-491.
  • 6Baugh, J.A., Chitnis, S., Donnelly, S.C., Monteiro, J., Lin, X., Plant, B.J., Wolfe, F., Gregersen, P.K., and Bucala, R. (2002). A functional promoter polymorphism in the macrophage migration inhibitory factor (M/F) gene associated with disease severity in rheumatoid arthritis. Genes Immun. 3: 170-176.
  • 7Bellamy, R. (2003). Susceptibility to mycobacterial infections: the importance of host genetics. Genes Immun. 4:4-11.
  • 8Biezeveld, M., Geissler, J., Merkus, M., Kuipers, I.M., Ottenkamp, J., and Kuijpers, T. (2006). The involvement of Fc gamma receptor gent polymorphisms in Kawasaki disease. Clin. Exp. Immunol. 147: 106-111.
  • 9Bloom, B.R., and Bennett, B. (1966). Mechanism of a reaction in vitro associated with delayed-type hypersensitivity. Science 153: 80-82.
  • 10Calandra, T. (2003). Macrophage migration inhibitory factor and host innate immune responses to microbes. Scand. J. Infect. Dis. 35: 573-576.

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