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溶组织内阿米巴:实验性诱导盲肠阿米巴病沙鼠(长爪沙鼠)的淋巴网状组织变化

Entamoeba histolytica: lymphoreticular changes in gerbils (Meriones unguiculatus) with experimentally induced cecal amebiasis.

作者信息

Chadee K, Meerovitch E

出版信息

J Parasitol. 1985 Oct;71(5):566-75.

PMID:2865345
Abstract

Antibody responses and changes in the lymphoreticular tissues of gerbils with experimental cecal amebiasis were studied from 5 to 60 days PI. Changes in the cecum consisted of lymphoid follicle hyperplasia and depletion of lymphocytes, followed by follicle atrophy and histiocytosis. Mesenteric lymphadenopathy, and histologic alterations in the lymph nodes paralleled the progressive development of amebic cecal lesions. Early in the infection (5 to 10 days PI) mesenteric lymph nodes showed cortical follicle hyperplasia, blastogenesis in the paracortical areas (PCA) and intense lymphoblast and plasma cell activity in the medullary cords. At 20 to 30 days PI, the cortical follicles, the PCA and the medulla were depleted of lymphocytes and there was histiocytosis throughout the organ. At 60 days PI, lymphocyte repopulation took place in the PCA, and cortical follicles had active germinal centers. Spleen follicles did not increase in number as the infection progressed, but became hyperplastic. Antibody titers to ameba were low throughout the cecal infection but rose whenever amebic metastasis to the liver occurred. The results of this study indicate that lymphocytes from the submucosal lymphoid follicles and the draining lymph nodes may control the pathogenesis of the infection. Lymphoreticular tissue alterations could result from antigenic stimulation and migration of cells to the sites of infection.

摘要

在感染后5至60天,对患有实验性盲肠阿米巴病的沙鼠的抗体反应和淋巴网状组织变化进行了研究。盲肠的变化包括淋巴滤泡增生和淋巴细胞耗竭,随后是滤泡萎缩和组织细胞增多。肠系膜淋巴结病以及淋巴结的组织学改变与阿米巴盲肠病变的进展平行。在感染早期(感染后5至10天),肠系膜淋巴结显示皮质滤泡增生、副皮质区(PCA)母细胞化以及髓索中强烈的淋巴母细胞和浆细胞活性。在感染后20至30天,皮质滤泡、PCA和髓质的淋巴细胞耗竭,整个器官出现组织细胞增多。在感染后60天,PCA中发生淋巴细胞再填充,皮质滤泡有活跃的生发中心。随着感染进展,脾滤泡数量未增加,但出现增生。在整个盲肠感染过程中,抗阿米巴抗体滴度较低,但每当发生阿米巴肝转移时滴度就会升高。本研究结果表明,来自黏膜下淋巴滤泡和引流淋巴结的淋巴细胞可能控制感染的发病机制。淋巴网状组织改变可能是由抗原刺激和细胞向感染部位迁移导致的。

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