Differential pattern of cytokine expression by macrophages infected in vitro with different Mycobacterium tuberculosis genotypes
Differential pattern of cytokine expression by macrophages infected in vitro with different Mycobacterium tuberculosis genotypes
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DOI：
10.1111/j.1365-2249.2005.02797.x
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发表时间：
2005-06-01
影响因子：
4.6
通讯作者：
Estrada-García, I
中科院分区：
文献类型：
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作者：
Chacón-Salinas, R;Serafín-López, J;Estrada-García, I
最近的研究表明，不同基因型的结核分枝杆菌在宿主中诱导不同的免疫应答，如细胞因子和iNOS表达的变化所反映的。由于这些分子在体内可能受到多种因素的调节，因此通过实时聚合酶链反应（PCR）和酶联免疫吸附试验（ELISA）评估细胞因子和iNOS表达，对这种复杂现象进行了部分分析，该模型采用三种不同的M.结核病基因型：Canetti、H37 Rv和Beijing。虽然这三种基因型诱导生产的iNOS和不同的细胞因子在感染后24小时进行测试，与其他基因型感染的细胞相比，与北京分离株感染的巨噬细胞表达最高水平的mRNA的iNOS，白细胞介素（IL）-1 β，肿瘤坏死因子（TNF）-α，IL-12细胞因子和较低水平的IL-10。这种表达模式与感染控制有关，但在体内感染北京基因型时，它在进展到慢性期时丢失。控制感染的失败可能受到疾病过程中其他细胞类型产生的细胞因子和细菌分子的影响。这项工作中提出的结果表明，每种基因型都有能力诱导不同水平的细胞因子表达，这可能与感染期间的发病机制有关。
It has been shown recently that different genotypes of Mycobacterium tuberculosis induce distinct immune responses in the host, as reflected by variations in cytokine and iNOS expression. Because these molecules are probably regulated by multiple factors in vivo this complex phenomenon was partially analysed by assessing cytokine and iNOS expression by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) in an in vitro model of bone marrow-derived macrophages infected with three different M. tuberculosis genotypes: Canetti, H37 Rv and Beijing. Although the three genotypes induced production of iNOS and the different cytokines tested at 24 h post-infection, macrophages infected with the Beijing isolate expressed the highest levels of mRNA for iNOS, interleukin (IL)-1 beta, tumour necrosis factor (TNF)-alpha, IL-12 cytokines and lower levels of IL-10 compared with cells infected with other genotypes. This expression pattern has been associated with infection control, but during infection in vivo with the Beijing genotype it is lost upon progression to chronic phase. The failure to control infection is likely to be influenced by cytokines produced by other cell types and bacterial molecules expressed during the course of disease. Results presented in this work show that each genotype has the ability to induce different levels of cytokine expression that could be related to its pathogenesis during infection.