Klei T R, McVay C S, Dennis V A, Coleman S U, Enright F M, Casey H W
Department of Veterinary Microbiology and Parasitology, School of Veterinary Medicine, Louisiana State University, Baton Rouge 70803.
Exp Parasitol. 1990 Nov;71(4):393-405. doi: 10.1016/0014-4894(90)90065-k.
The effects of Brugia pahangi infection duration and parasite burden on parasite-associated inflammatory and immune responses were determined over a 181-day period in jirds receiving from one to eight inoculations of infective larvae. Multiple infections did not produce a protective resistance to reinfection as determined by adult worm recovery at necropsy. Intralymphatic granulomatous lesions, lymph thrombi, were first seen at 48 days post initial inoculation (DPI). The numbers of lymph thrombi reached peak levels in singly inoculated jirds at 90 DPI and significantly decreased to low levels by 160 DPI. The ratio of lymph thrombi to adult worms recovered from the spermatic cord lymphatics followed a similar pattern. Sizes of renal lymph nodes, which drain lymphatics containing parasites, followed a temporal pattern of increase and decrease similar to that of lymph thrombi numbers. Peak granuloma areas around antigen-coated beads embolized in lungs were seen at 27 DPI. Granuloma areas around antigen-coated beads began to decrease after 69 DPI and reached sizes not significantly different from uninfected controls by 118 DPI. Multiple inoculations of infective larvae and increasing worm burdens did not affect the pattern of granulomatous response to antigen-coated beads. Eosinophilia of singly and multiply infected jirds peaked at 26 DPI. Eosinophilia of singly infected jirds returned to normal levels by 103 DPI but those of multiply infected jirds remained elevated until 160 DPI. Lymph node cell blastogenic responses to antigen were greater than those of splenocytes at all time intervals measured. However, significant differences in stimulation indexes between groups with different infection durations were not seen with either cell type. Antibody responses to somatic adult worm antigen as measured by ELISA reached near peak levels by 48 DPI and remained elevated for the course of the study in all infected jirds. The decrease in lymphatic lesion severity seen in chronically infected jirds temporally corresponds to the decrease in granulomatous reactivity measured around antigen-coated beads embolized in the lungs. This observation suggests that host and/or parasite factors associated with these two phenomena may be similar. Although these decreases may be the result of down-regulated immune responses, corresponding decreases in antibody levels and blastogenesis of lymphocytes stimulated by crude worm extracts were not observed in chronic infections.
在181天的时间里，对接受1至8次感染性幼虫接种的沙鼠进行研究，以确定彭亨布鲁线虫感染持续时间和寄生虫负荷对寄生虫相关炎症和免疫反应的影响。尸检时通过成虫回收情况确定，多次感染并未产生对再感染的保护性抵抗力。初次接种后48天（DPI）首次观察到淋巴管内肉芽肿性病变，即淋巴血栓。在单次接种的沙鼠中，淋巴血栓数量在90 DPI时达到峰值水平，并在160 DPI时显著降至低水平。从精索淋巴管回收的淋巴血栓与成虫的比例遵循类似模式。引流含有寄生虫淋巴管的肾淋巴结大小呈现出与淋巴血栓数量相似的先增加后减少的时间模式。在肺中栓塞的抗原包被珠周围的肉芽肿面积在27 DPI时达到峰值。69 DPI后，抗原包被珠周围的肉芽肿面积开始减小，到118 DPI时达到与未感染对照组无显著差异的大小。多次接种感染性幼虫和增加虫负荷并未影响对抗原包被珠的肉芽肿反应模式。单次和多次感染的沙鼠嗜酸性粒细胞增多在26 DPI时达到峰值。单次感染沙鼠的嗜酸性粒细胞增多在103 DPI时恢复到正常水平，但多次感染沙鼠的嗜酸性粒细胞增多一直持续到160 DPI。在所有测量的时间间隔内，淋巴结细胞对抗原产生的增殖反应均大于脾细胞。然而，不同感染持续时间组之间，两种细胞类型的刺激指数均未观察到显著差异。通过ELISA测量，对成虫体抗原的抗体反应在48 DPI时接近峰值水平，并在所有感染沙鼠的研究过程中一直保持升高。在慢性感染的沙鼠中观察到的淋巴管病变严重程度的降低，在时间上与在肺中栓塞的抗原包被珠周围测量的肉芽肿反应性降低相对应。这一观察结果表明，与这两种现象相关的宿主和/或寄生虫因素可能相似。尽管这些降低可能是免疫反应下调的结果，但在慢性感染中未观察到抗体水平和粗制虫提取物刺激的淋巴细胞增殖相应降低。
