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首页> 美国卫生研究院文献>Infection and Immunity >DNA from Protozoan Parasites Babesia bovis Trypanosoma cruzi and T. brucei Is Mitogenic for B Lymphocytes and Stimulates Macrophage Expression of Interleukin-12 Tumor Necrosis Factor Alpha and Nitric Oxide
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DNA from Protozoan Parasites Babesia bovis Trypanosoma cruzi and T. brucei Is Mitogenic for B Lymphocytes and Stimulates Macrophage Expression of Interleukin-12 Tumor Necrosis Factor Alpha and Nitric Oxide

机译：来自原生动物寄生虫牛肝杆菌克氏锥虫和布氏锥虫的DNA对B淋巴细胞具有成丝性并刺激白细胞介素12肿瘤坏死因子α和一氧化氮的巨噬细胞表达。

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The activation of innate immune responses by genomic DNA from bacteria and several nonvertebrate organisms represents a novel mechanism of pathogen recognition. We recently demonstrated the CpG-dependent mitogenic activity of DNA from the protozoan parasite Babesia bovis for bovine B lymphocytes (W. C. Brown, D. M. Estes, S. E. Chantler, K. A. Kegerreis, and C. E. Suarez, Infect. Immun. 66:5423–5432, 1998). However, activation of macrophages by DNA from protozoan parasites has not been demonstrated. The present study was therefore conducted to determine whether DNA from the protozan parasites B. bovis, Trypanosoma cruzi, and T. brucei activates macrophages to secrete inflammatory mediators associated with protective immunity. DNA from Escherichia coli and all three parasites stimulated B-lymphocyte proliferation and increased macrophage production of interleukin-12 (IL-12), tumor necrosis factor alpha (TNF-α), and nitric oxide (NO). Regulation of IL-12 and NO production occurred at the level of transcription. The amounts of IL-12, TNF-α, and NO induced by E. coli and protozoal DNA were strongly correlated (r2 > 0.9) with the frequency of CG dinucleotides in the genome, and immunostimulation by DNA occurred in the order E. coli ≥ T. cruzi > T. brucei > B. bovis. Induction of inflammatory mediators by E. coli, T. brucei, and B. bovis DNA was dependent on the presence of unmethylated CpG dinucleotides. However, at high concentrations, E. coli and T. cruzi DNA-mediated macrophage activation was not inhibited following methylation. The recognition of protozoal DNA by B lymphocytes and macrophages may provide an important innate defense mechanism to control parasite replication and promote persistent infection.
机译：来自细菌和几种非脊椎动物的基因组DNA对先天免疫应答的激活代表了病原体识别的新机制。我们最近证明了来自原生动物寄生虫牛肝杆菌的DNA对牛B淋巴细胞的CpG依赖性有丝分裂活性（WC Brown，DM Estes，SE Chantler，KA Kegerreis和CE Suarez，Infect。Immun。66：5423–5432，1998） 。但是，尚未证明原生动物寄生虫通过DNA激活巨噬细胞。因此，进行本研究以确定来自原生动物寄生虫牛牛，牛锥虫和布氏锥虫的DNA是否能激活巨噬细胞分泌与保护性免疫有关的炎症介质。大肠杆菌和所有三个寄生虫的DNA刺激B淋巴细胞增殖，并增加白细胞介素12（IL-12），肿瘤坏死因子α（TNF-α）和一氧化氮（NO）的巨噬细胞生成。 IL-12和NO产生的调节发生在转录水平。大肠杆菌和原生动物DNA诱导的IL-12，TNF-α和NO的量与基因组中CG二核苷酸的频率和免疫刺激密切相关（r 2 布氏梭菌>牛双歧杆菌。大肠杆菌，布鲁氏杆菌和牛双歧杆菌DNA诱导炎性介质取决于未甲基化的CpG二核苷酸的存在。但是，在高浓度下，甲基化后，大肠杆菌和克鲁维酵母DNA介导的巨噬细胞活化并未受到抑制。 B淋巴细胞和巨噬细胞对原生动物DNA的识别可能提供重要的先天防御机制，以控制寄生虫复制并促进持续感染。

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