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海鱼分枝杆菌在T细胞耗竭小鼠脚垫中的生长。

Growth of Mycobacterium marinum in the footpads of T-cell-depleted mice.

作者信息

Collins F M, Montalbine V, Morrison N E

出版信息

Infect Immun. 1975 May;11(5):1088-93. doi: 10.1128/iai.11.5.1088-1093.1975.

Abstract

Mycobacterium marinum strains 1218 and 1219 were inoculated into the hind footpads of T-cell-depleted specific pathogen-free C57B1/6 mice, and the growth and survival of the organisms at the site of injection, the draining popliteal lymph node, and the spleen and lung were quantitated for up to 70 days. T-cell depletion largely ablated the normal cell-mediated antituberculous response to the M. marinum population. The mice were able to control the further growth of the inoculum within the footpad only after it had reached 5 to 10 times that present in the normal controls. The high temperature-adapted strain (37 C; strain no. 1218) induced an increasing infection in the liver, spleen, and lungs of the THXB mice, and the infection eventually spread to the opposite footpad and to the tail skin. Strain 1219 gave rise to considerable systemic involvement in the THXB host despite its inability to survive at 37 C, but the size of the splenic and lung populations was considerably lower than in the 1218-infected animals. Both M. marinum infections persisted in the tissues of the T-cell-depleted mice with no indication of a cell-mediated immune response. Footpad swelling in the M. marinum-infected mice was not greatly reduced by T-cell depletion, and, if anything, tended to persist at high levels long after the swelling of the control feet had gone into a decline. On the other hand, incorporation of tritiated thymidine by cells within the infected footpads, the draining lymph node, and the spleen was considerably reduced in the T-cell-depleted host compared with control values. Late in the infection, there was a significant increase in the amount of label taken up by the cells in the footpads of the T-cell-depleted host.

摘要

将海分枝杆菌菌株1218和1219接种到T细胞耗竭的无特定病原体C57B1/6小鼠的后足垫中,对注射部位、引流腘窝淋巴结、脾脏和肺中该菌的生长和存活情况进行长达70天的定量分析。T细胞耗竭在很大程度上消除了对海分枝杆菌群体正常的细胞介导的抗结核反应。只有在接种物数量达到正常对照的5至10倍后,小鼠才能控制其在足垫内的进一步生长。高温适应菌株(37℃;菌株编号1218)在THXB小鼠的肝脏、脾脏和肺中引起的感染不断增加,最终感染扩散到对侧足垫和尾部皮肤。尽管菌株1219在37℃下无法存活,但在THXB宿主中仍引起了相当程度的全身感染,但其在脾脏和肺中的菌量明显低于感染1218菌株的动物。两种海分枝杆菌感染在T细胞耗竭小鼠的组织中持续存在,但未显示出细胞介导的免疫反应迹象。T细胞耗竭并没有使感染海分枝杆菌小鼠的足垫肿胀明显减轻,相反,在对照足垫肿胀消退很久之后,其足垫肿胀仍倾向于维持在较高水平。另一方面,与对照值相比,T细胞耗竭宿主中感染足垫、引流淋巴结和脾脏内细胞的氚化胸腺嘧啶核苷掺入量明显减少。在感染后期,T细胞耗竭宿主足垫中细胞摄取的标记物量显著增加。

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