Cholera enterotoxin (choleragen).
Cholera enterotoxin (choleragen).
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霍乱肠毒素（choleragen）。
DOI：
10.1016/0163-7258(85)90063-4
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发表时间：
1985
影响因子：
13.5
通讯作者：
Dorner,F
中科院分区：
文献类型：
--
作者：
Finkelstein,RA;Dorner,F
许多报告和观察导致了霍乱毒素知识的现状，这些报告和观察在其他地方进行了广泛的总结（Pollitzer，1959; Finkelstein，1973，1975）。1976，1981，1984; Barua和Burrows，1974;班尼特和Cuatrecasas，1977; Gill，1978; Moss和Vaughan，1979; Ouchterlony和Holmgren，1980; Holmgren，1981; Giannella，1981; Gill，1982; S.货车Heyningen，1982; Moss和Vaughan，1982;货车Heyningen和Seal，1983）。由于这个原因，这次审查将主要限于一个一般性的描述，以及霍乱研究的最新进展的总结。霍乱毒素是在科赫于世纪末（参见Pollitzer，1959）预测霍乱是一种毒素介导的疾病之后近75年才被“发现”的。支持这一预测的合理数据首次出现在1959年，当时两名印度研究人员相互独立地工作，表明来自霍乱弧菌的无细胞制剂在他们开发的动物模型中引起相关的腹泻病（De，1959; Dutta等人，1959年）。一种模型是成年家兔结扎回肠袢（De和Chatterje，1953），其对一种未鉴定的Ogawa血清型霍乱弧菌菌株的无菌培养物有反应，并伴有管腔液体蓄积，表明具有“肠毒性”（De，t959）。另一个模型（Dutta和Habbu，1955）是幼兔，当喂食多剂量的569 B Inaba霍乱弧菌菌株重悬液的无菌裂解物时（Durra等人，1959年），以致死性霍乱性腹泻应答。到1964年，已经证明，通过在补充有酪蛋白氨基酸的合成培养基（Finkelstein和Lankford，1955）中在剧烈通气下生长菌株569 B Inaba，可以常规地和最佳地产生肠毒性活性（Finkelstein等人，1964年）。假定的霍乱肠毒素，这是证明不是霍乱内毒素，然后被命名为choleragen-现在是一个公认的同义词（Stedman's Medical Dictionary，1972）Dorland's Medical Dictionary，1974）用于霍乱毒素（CT）或霍乱肠毒素。在随后的几年里，作为对霍乱基础研究的产物以及由此产生的对其病理生理学的理解的增加，已经发展出一种经济有效的治疗疟疾的方法----口服体液补充疗法（ORT）（世界卫生组织，1983年）。口服体液补充疗法被认为可能是世纪最重要的医学进步，仅在1980年代的十年中就将挽救无数人的生命。然而，完全令人满意的方法，预防疾病或中断其进展，当它发生时，仍然有待开发。
The many reports and observations that have led to the current state of knowledge of cholera toxin have been summarized extensively elsewhere (Pollitzer, 1959; Finkelstein, 1973, 1975. 1976, 1981, 1984; Barua and Burrows, 1974; Bennett and Cuatrecasas, 1977; Gill, 1978; Moss and Vaughan, 1979; Ouchterlony and Holmgren, 1980; Holmgren, 1981; Giannella, 1981; Gill, 1982; S. van Heyningen, 1982; Moss and Vaughan, 1982; van Heyningen and Seal, 1983). For this reason this review will be confined primarily to a general description as well as a summary of recent progress in cholera research. Cholera toxin was' discovered'nearly 75 years after Koch's prediction, in the late 19th century (see Pollitzer, 1959), that cholera is a toxin-mediated disease. Reasonable data to support this prediction first became available in 1959 when two Indian researchers, working independently of one another, showed that cell-free preparations from Vibrio cholerae caused relevant symptomatology in animal models which they had developed (De, 1959; Dutta et al., 1959). One model was the adult rabbit ligated ileal loop (De and Chatterje, 1953) which responded to sterile culture filtrates of an unidentified Ogawa serotype strain of V. cholerae with luminal fluid accumulation which suggested'enterotoxicity'(De, t959). The other model (Dutta and Habbu, 1955) was the infant rabbit which, when fed multiple doses of sterile lysates of heavy suspensions of the 569B Inaba strain of V. cholerae (Durra et al., 1959), responded with fatal choleraic diarrhea. By 1964 it had been demonstrated that enterotoxic activity could be produced routinely and optimally by growing strain 569B Inaba with vigorous aeration in synthetic culture medium (Finkelstein and Lankford, 1955) supplemented with casamino acids (Finkelstein et al., 1964). The putative cholera enterotoxin, which was shown not to be the cholera endotoxin, was then named choleragen--now an accepted synonym (Stedman's Medical Dictionary, 1972; Dorland's Medical Dictionary, 1974) for cholera toxin (CT) or cholera enterotoxin.In subsequent years, as an outgrowth of basic research on cholera and the resulting increased understanding of its pathophysiology, a simple, economical and effective treatment regimen for diarrheal disease has been developed--oral rehydration therapy (ORT)(World Health Organization, 1983). Regarded as potentially the most important medical advance of the century, ORT will save countless millions of lives in the decade of the 1980s alone. However, completely satisfactory methods of preventing the disease or of interrupting its progress, when it occurs, remain to be developed.