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趋化因子在重症继发性肺结核患者表达研究

, PP. 415-419

Keywords: ,结核,趋化因子,聚合酶链反应

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Abstract:

目的对基因表达谱芯片筛选出的重症比对轻症继发性肺结核患者基因CCL3、CCL4、CXCL2进行验证,探索其表达下调与重症继发性肺结核免疫病理机制的关系。方法用Affymetrix基因表达谱芯片检测重症和轻症继发性肺结核患者以及与健康对照相比的差异表达基因;用real-timePCR法测定重症、轻症患者和健康对照CCL3、CCL4、CXCL2的相对表达量;用方差分析和非参数检验统计方法判断组间比较的统计学意义。结果表达谱芯片筛选出重症继发性肺结核患者有大量差异表达基因,一些免疫基因表现为下调,可能与病变严重程度有相关性。real-timePCR结果显示CCL3在重症vs轻症表达下调(PP<0.05)。结论基因表达谱芯片检测CCL3、CCL4、CXCL2在重症vs轻症继发性肺结核患者表达下调,验证结果与芯片基本相符,趋化因子下调可能在重症继发性肺结核免疫病理机制中有重要作用。

References

[1]  中华医学会.临床诊疗手册(结核病分册)[M].北京:人民卫生出版社,2005:7-10.
[2]  刘同伦. 实用结核病学[M]. 沈阳: 辽宁科学技术出版社, 1987.284-289.
[3]  Dlugocitzky D, Bay ML, Rateni L, et al. Influence of disease severity on nitrite and cytokine production by peripheral blood mononuclear cells (PBMC) from patients with pulmonary tuberculosis (TB) [J]. Clin Exp Immunol .2000, 122(3):343-349.
[4]  王琳,蔡映云,程秋兰,等.肺结核患者的Th1/Th2细胞因子失衡[J].中华结核和呼吸杂志. 2002,25(9): 535-537.
[5]  Ehrlich RI, Adams S, Baatjies R, et al. Chronic airflow obstruction and respiratory symptoms following tuberculosis: a review of South African studies [J]. Int J Tuberc Lung Dis, 2011,15: 886-891.
[6]  施雯慧, 陈伟. 结核病发病影响因素研究进展 [J]. 中华流行病学杂志, 2012, 33(12): 1296-1300.
[7]  Orme IM, Basaraba RJ. The formation of the granuloma in tuberculosis infection[J]. Semin Immunol, 2014 ,26(6):601-609.
[8]  Slight SR, Khader SA.Chemokines shape the immune responses to tuberculosis[J]. Cytokine Growth Factor Rev, 2013,24(2):105-113.
[9]  Van Sweringen HL, Sakai N, Tevar AD,et al.CXC chemokine signaling in the liver: Impact on repair and regeneration[J]. Hepatology, 2011,54(4): 1445-1453.
[10]  Rajan D, McCracken CE, Kopleman HB,et al. Human rhinovirus induced cytokine/chemokine responses in human airway epithelial and immune cells[J].PLoS One,2014, 9(12): e114322.
[11]  Hilda JN, Narasimhan M, Das SD. Neutrophils from pulmonary tuberculosis patients show augmented levels of chemokines MIP-1α, IL-8 and MCP-1 which further increase upon in vitro infection with mycobacterial strains[J]. Hum Immunol, 2014,75(8):914-22.
[12]  Das S, Banerjee S, Majumder S, et al.Immune Subversion by Mycobacterium tuberculosis through CCR5 Mediated Signaling: Involvement of IL-10[J]. PLoS One. 2014; 9(4): e92477.
[13]  Monin L, Khader SA. Chemokines in tuberculosis: The good, the bad and the ugly[J]. Semin Immunol, 2014,26(6):552-558.
[14]  Lyadova IV, Tsiganov EN, Kapina MA. In mice, tuberculosis progression is associated with intensive inflammatory response and the accumulation of Gr-1 cells in the lungs[J]. PLoS One, 2010,5(5):e10469.
[15]  Strieter RM, Gomperts BN, Keane MP. The role of CXC chemokines in pulmonary fibrosis[J] .J Clin Invest, 2007, 117(3): 549-556.
[16]  Aly S, Laskay T, Mages J, et al. Interferon-gamma-dependent mechanisms of mycobacteria-induced pulmonary immunopathology: the role of angiostasis and CXCR3-targeted chemokines for granuloma necrosis[J]. J Pathol. 2007 ,212(3):295-305.

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