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.
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