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特异性抗体和补体对溶组织内阿米巴滋养体运动性和生存力的影响。

The influence of specific antibodies and complement on the motility and the viability of Entamoeba histolytica trophozoites.

作者信息

Aust Kettis A, Utter G

出版信息

Am J Trop Med Hyg. 1984 Jul;33(4):569-77. doi: 10.4269/ajtmh.1984.33.569.

DOI:10.4269/ajtmh.1984.33.569
PMID:6089600
Abstract

The distribution of peroxidase-labeled normal or specific rabbit immunoglobulin (Ig) in Entamoeba histolytica trophozoites was studied by transmission electron microscopy. Small amounts of normal Ig became attached to the cell surface but did not redistribute. Internalized specific Ig was firmly bound to the inner membranes of phagocytosis vacuoles, while aggregates of normal Ig were dispersed over the vacuolar lumen. The distribution of fluorescein isothiocyanate-labeled Ig in living amebae was correlated with the cell motility at different times. Immobilization coincided with the cellular metabolic processing of internalized material. Remobilization occurred when the Ig was degraded and antibodies again bound to the reappearing surface antigens. E. histolytica activated complement by the classical pathway. Fresh guinea pig serum alone did not produce lysis which, however, did occur when it was added together with normal rabbit Ig. Normal rabbit Ig may constitute a complement-fixing substrate and activate complement by the classical pathway. Immobilization of the amebae by cytochalasin B (10 micrograms/ml) increased the susceptibility to cytolytic effects of specific antibodies or complement, or both. Pharmacological inhibition of cell motility might augment the immunological defence of the host against amebic infection.

摘要

利用透射电子显微镜研究了过氧化物酶标记的正常或特异性兔免疫球蛋白(Ig)在溶组织内阿米巴滋养体中的分布情况。少量正常Ig附着于细胞表面,但未重新分布。内化的特异性Ig牢固地结合在吞噬泡的内膜上,而正常Ig聚集体则分散在泡腔内。异硫氰酸荧光素标记的Ig在活阿米巴中不同时间的分布与细胞运动性相关。固定化与内化物质的细胞代谢过程一致。当Ig被降解且抗体再次结合到重新出现的表面抗原时,重新运动发生。溶组织内阿米巴通过经典途径激活补体。单独的新鲜豚鼠血清不会产生细胞溶解作用,然而,当它与正常兔Ig一起添加时则会发生细胞溶解。正常兔Ig可能构成一种补体结合底物,并通过经典途径激活补体。用细胞松弛素B(10微克/毫升)固定阿米巴会增加其对特异性抗体或补体或两者细胞溶解作用的敏感性。对细胞运动性的药理学抑制可能会增强宿主对阿米巴感染的免疫防御。

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Infect Immun. 1993 Mar;61(3):1048-54. doi: 10.1128/iai.61.3.1048-1054.1993.