Finkelstein R A, Boesman-Finkelstein M, Chang Y, Häse C C
Department of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia 65212.
Infect Immun. 1992 Feb;60(2):472-8. doi: 10.1128/iai.60.2.472-478.1992.
The structural gene, hap, for the secreted hemagglutinin/protease (HA/protease), a putative virulence factor of Vibrio cholerae, has recently been cloned and sequenced (C. C. Häse and R. A. Finkelstein, J. Bacteriol. 173:3311-3317, 1991). The availability of the null mutant, HAP-1, and HAP-1 complemented with pCH2 (which expresses HA/protease), enabled an examination of the role of HA/protease in the virulence of V. cholerae in an animal model. However, the mutants exhibited reversible colonial variation similar but not identical to that which was previously associated with dramatic changes in virulence of parental strain 3083. Regardless of colonial morphology, the mutants were found to be fully virulent in infant rabbits. Thus, the HA/protease is not a primary virulence factor (for infant rabbits). Observations using cultured human intestinal cells indicated, instead, that the HA/protease is responsible for detachment of the vibrios from the cultured cells by digestion of several putative receptors for V. cholerae adhesins.
霍乱弧菌假定的毒力因子——分泌型血凝素/蛋白酶(HA/蛋白酶)的结构基因hap,最近已被克隆和测序(C.C.哈泽和R.A.芬克尔斯坦,《细菌学杂志》173:3311 - 3317,1991年)。空突变体HAP - 1以及用pCH2(表达HA/蛋白酶)互补的HAP - 1的获得,使得能够在动物模型中研究HA/蛋白酶在霍乱弧菌毒力中的作用。然而,这些突变体表现出可逆的菌落变异,与之前与亲本菌株3083毒力显著变化相关的变异相似但不完全相同。无论菌落形态如何,这些突变体在幼兔中被发现具有完全的毒力。因此,HA/蛋白酶不是(针对幼兔的)主要毒力因子。相反,使用培养的人肠道细胞进行的观察表明,HA/蛋白酶通过消化霍乱弧菌粘附素的几种假定受体,负责使弧菌从培养细胞上脱离。