SUSCEPTIBLE MICE PRESENT HIGHER MACROPHAGE ACTIVATION THAN RESISTANT MICE DURING INFECTIONS WITH MYOTROPIC STRAINS OF TRYPANOSOMA-CRUZI
SUSCEPTIBLE MICE PRESENT HIGHER MACROPHAGE ACTIVATION THAN RESISTANT MICE DURING INFECTIONS WITH MYOTROPIC STRAINS OF TRYPANOSOMA-CRUZI
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DOI：
10.1111/j.1365-3024.1989.tb00675.x
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发表时间：
1989-07-01
影响因子：
2.2
通讯作者：
HONTEBEYRIEJOSKOWICZ, M
中科院分区：
文献类型：
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作者：
RUSSO, M;STAROBINAS, N;HONTEBEYRIEJOSKOWICZ, M
在已知对克氏锥虫嗜肌性菌株（Colombian和CL）感染的相对抗性不同的近交系小鼠（C3 H、BALB、B6和B10.A）之间比较巨噬细胞活化的动力学。用于测量巨噬细胞活化的参数是在玻璃表面上的快速扩散、过氧化氢释放和肿瘤坏死因子/恶病质产生。从感染两种菌株的C3 H（可感染）、BALB（中间）和B6或B10.A（抗性）小鼠获得的巨噬细胞。克鲁齐氏病在寄生虫病发作时开始迅速传播。令人惊讶的是，从更易感的小鼠品系（C3 H）获得的腹膜细胞释放的过氧化氢的量显著高于其他小鼠品系。此外，仅在C3 H小鼠的血清中检测到肿瘤坏死因子/恶病质。这些结果表明，对嗜肌性T。Cruzi与增强的巨噬细胞活化无关。它还表明，获得性巨噬细胞活化在很大程度上依赖于T-淋巴细胞轴承的表型标记CD 4（辅助/诱导），因为所有参数的巨噬细胞活化显着抑制在无胸腺小鼠或C3 H小鼠在体内治疗的单克隆抗体抗CD 4 + T细胞。
The kinetics of macrophage activation were compared among inbred strains of mice (C3H, BALB, B6 and B10.A) that are known to differ in their relative resistance to infections with the myotropic strains (Colombian and CL) of Trypanosoma cruzi. The parameters utilized to measure macrophage activation were rapid spreading on glass surfaces, hydrogen peroxide release and tumour necrosis factor/cachectin production. Macrophages obtained from C3H (susceptibile), BALB (intermediate) and B6 or B10.A (resistant) mice infected with both strains of T. cruzi began to spread rapidly at the onset of parasitaemia. Surprisingly, the amount of hydrogen peroxide released by peritoneal cells obtained from the more susceptible mouse strain (C3H) was significantly higher than in the other mouse strains. Also, only in the serum of C3H mice was tumour necrosis factor/cachectin detected. These results suggest that resistance against infections with myotropic strains of T. cruzi does not correlate with enhanced macrophage activation. It is also shown that the acquired macrophage activation is largely dependent on T-lymphocytes bearing the phenotypic marker CD4 (helper/inducer), since all parameters of macrophage activation were significantly inhibited in athymic mice or in C3H mice treated in vivo with monoclonal antibody anti-CD4+ T-cells.