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十足目甲壳动物肝胰腺的细胞病理学与免疫反应

Cytopathology and immune response in the hepatopancreas of decapod crustaceans.

作者信息

Vogt Günter

机构信息

Faculty of Biosciences, University of Heidelberg, Im Neuenheimer Feld 234, 69120 Heidelberg, Germany.

出版信息

Dis Aquat Organ. 2020 Feb 27;138:41-88. doi: 10.3354/dao03443.

DOI:10.3354/dao03443
PMID:32103822
Abstract

The hepatopancreas of decapod crustaceans is used as an example to illustrate the range of cytopathologies, detoxification mechanisms, and immune responses that environmental toxicants and pathogens can induce in a single organ. The hepatopancreas is the central metabolic organ of decapods and consists of hundreds of blindly-ending tubules and intertubular spaces. The tubular epithelium contains 5 structurally and functionally different cell types, and the interstitium contains haemolymph, haemocytes, connective tissue, and fixed phagocytes. Some physiological conditions such as moulting and starvation cause marked but reversible ultrastructural alterations of the epithelial cells. Environmental toxicants induce either detoxification mechanisms or structural damage in cells, depending on toxicant and concentration. The hepatopancreas is also a main target organ for pathogens, mainly viruses, bacteria, and protists that enter the body via the digestive tract and gills and replicate in the hepatopancreatocytes. The cytopathologies caused by toxicants and pathogens affect single cell types specifically or, more often, several cell types simultaneously. Pathogenesis often begins in a certain cell organelle such as the nucleus, mitochondrion, or endoplasmic reticulum, spreads to other organelles, and ends with death of the infected cell. Fixed phagocytes in the interstitium capture and degrade pathogens that move from the infected tubules into the intertubular spaces or enter the hepatopancreas via circulation. Relatively few disease agents elicit the melanisation and encapsulation reaction that encloses infected tubules by a rigid melanised capsule and kills the entrapped pathogens.

摘要

十足目甲壳动物的肝胰腺被用作一个例子,来说明环境毒物和病原体在单个器官中可诱导产生的一系列细胞病变、解毒机制和免疫反应。肝胰腺是十足目动物的中央代谢器官,由数百个盲端小管和小管间间隙组成。管状上皮包含5种结构和功能不同的细胞类型,间质包含血淋巴、血细胞、结缔组织和固定吞噬细胞。一些生理状况,如蜕皮和饥饿,会导致上皮细胞出现明显但可逆的超微结构改变。环境毒物会根据毒物种类和浓度,在细胞中诱导解毒机制或造成结构损伤。肝胰腺也是病原体的主要靶器官,主要是通过消化道和鳃进入体内并在肝胰腺细胞中复制的病毒、细菌和原生生物。毒物和病原体引起的细胞病变会特异性地影响单一细胞类型,或者更常见的是同时影响几种细胞类型。发病过程通常始于某个细胞器,如细胞核、线粒体或内质网,扩散到其他细胞器,最终导致受感染细胞死亡。间质中的固定吞噬细胞捕获并降解从受感染小管进入小管间间隙或通过循环进入肝胰腺的病原体。相对较少的病原体能引发黑化和包囊反应,即通过坚硬的黑化包囊包围受感染的小管并杀死被困在其中的病原体。

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