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首页> 外文期刊>Infection and immunity >Protein Deficiency Induces Alterations in the Distribution of T-Cell Subsets in Experimental Pulmonary Tuberculosis
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Protein Deficiency Induces Alterations in the Distribution of T-Cell Subsets in Experimental Pulmonary Tuberculosis

机译：蛋白质缺乏症诱发实验性肺结核中T细胞亚群分布的变化

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Previous research has suggested that dietary protein deficiency alters resistance to experimental pulmonary tuberculosis, in part, by affecting the distribution and trafficking of antigen-reactive T cells. In this study, guinea pigs were maintained on either a protein-deficient (10% ovalbumin) or control (30% ovalbumin) diet and infected 4 to 6 weeks later with a low dose of virulentMycobacterium tuberculosis H37Rv by the respiratory route. Monoclonal antibodies directed against the CD4 or CD8 markers on guinea pig lymphocytes were used in a flow cytofluorometric assay to determine the proportion of each subset in the peripheral circulation, spleen, and bronchotracheal lymph nodes at 4 weeks after infection. In uninfected guinea pigs, only the spleen exhibited an effect of diet on T-cell distribution, with small but consistent reductions in the proportions of both CD4 and CD8 T lymphocytes. However, following infection, protein deficiency exerted a profound effect on T-cell distribution. Malnourished, tuberculous guinea pigs harbored only 20 and 60% of the T cells (as a proportion of total lymphoid cells) found in the spleen and blood, respectively, of their well-nourished counterparts. Normal relative proportions of CD4 and CD8 cells were observed, however. In striking contrast, the bronchotracheal lymph nodes of protein-deprived guinea pigs with tuberculosis contained more than twice the numbers of T cells of control guinea pigs, and the normal CD4-to-CD8 ratio was reversed. Peripheral T-cell function, as measured by the delayed hypersensitivity skin test to tuberculin, and antigen-induced lymphoproliferation in vitro were markedly suppressed in protein-malnourished animals. Conversely, purified protein derivative-induced (but not concanavalin A-induced) proliferation was significantly enhanced in cultures of lymph node cells from protein-deprived tuberculous animals. Taken together, these results suggest that immunological abnormalities and loss of antimycobacterial resistance in the lungs of protein-deficient guinea pigs may be explained, in part, by sequestration of antigen-reactive T cells in the lymph nodes draining the site of infection.
机译：先前的研究表明，饮食中蛋白质缺乏会部分地通过影响抗原反应性T细胞的分布和运输而改变对实验性肺结核的抵抗力。在这项研究中，豚鼠维持蛋白质缺乏（10％卵清蛋白）或对照（30％卵清蛋白）饮食，并在4至6周后用低剂量的强力结核分枝杆菌 H37Rv感染通过呼吸途径。针对豚鼠淋巴细胞上CD4或CD8标记的单克隆抗体用于流式细胞荧光分析，以确定感染后4周时外周循环，脾脏和支气管气管淋巴结中每个子集的比例。在未感染的豚鼠中，只有脾脏对T细胞分布具有饮食效果，而CD4和CD8 T淋巴细胞的比例却有少量但持续的降低。然而，感染后，蛋白质缺乏对T细胞分布产生了深远的影响。营养不良的结核豚鼠仅在其脾脏和血液中分别含有20％和60％的T细胞（占总淋巴样细胞的比例）。然而，观察到CD4和CD8细胞的正常相对比例。与之形成鲜明对比的是，患有蛋白质缺乏症的豚鼠结核病的支气管气管淋巴结中含有的T细胞数量是对照豚鼠的T细胞数量的两倍以上，并且正常的CD4与CD8的比例相反。在蛋白质营养不良的动物中，外周血T细胞功能（通过对结核菌素的迟发性超敏性皮肤试验测定）和抗原诱导的体外淋巴细胞增殖在体外得到了显着抑制。相反，在缺乏蛋白质的结核动物的淋巴结细胞培养物中，纯化的蛋白衍生物诱导的（但不是伴刀豆球蛋白A诱导的）增殖显着增强。综上所述，这些结果表明，蛋白质缺乏的豚鼠的肺部免疫异常和抗分枝杆菌抗性的丧失可能部分地通过隔离排泄感染部位的淋巴结中的抗原反应性T细胞得以解释。

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