Genome sequence of Vibrio parahaemolyticus:: a pathogenic mechanism distinct from that of V cholerae
Genome sequence of Vibrio parahaemolyticus:: a pathogenic mechanism distinct from that of V cholerae
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DOI：
10.1016/s0140-6736(03)12659-1
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发表时间：
2003-03-01
期刊：
影响因子：
168.9
通讯作者：
Iida, T
中科院分区：
文献类型：
--
作者：
Makino, K;Oshima, K;Iida, T
副溶血性弧菌是一种革兰氏阴性海洋细菌，是世界范围内引起食源性胃肠炎的原因。几种特定血清型的副溶血性V毒株，可能来源于一个共同的克隆祖先，最近引起了胃肠炎大流行。这种生物在系统发育上与霍乱的病原体霍乱弧菌接近。方法采用散弹枪测序法建立临床副溶血性V病毒RIMD2210633株的全基因组序列。利用Gambler和Glimmer程序对编码序列进行了识别。用MUMmer与霍乱弧菌基因组进行了比较分析。发现基因组由2条圆形染色体组成，分别为3 288 558 bp和1877 212 bp；它包含4832个基因。副溶血性V病毒基因组与霍乱V病毒基因组的比较显示，两条染色体内部和之间有许多重排。在副溶血性V病毒基因组中鉴定出III型分泌系统（TTSS）基因；霍乱弧菌没有这些基因。TTSS是引起腹泻的细菌（如志贺氏菌、沙门氏菌和肠致病性大肠杆菌）的主要毒力因子，这些细菌通过侵入肠上皮细胞或与肠上皮细胞密切相互作用而引起胃肠炎。我们的研究结果表明，副溶血性弧菌和霍乱弧菌通过不同的机制建立感染。这一发现解释了副溶血性V菌感染的临床特征，通常包括炎症性腹泻，在某些情况下还包括败血症等全身性表现，这与通常与非炎症性腹泻相关的霍乱V菌感染不同。
Background Vibrio parahaemolyticus, a gram-negative marine bacterium, is a worldwide cause of food-borne gastroenteritis. V parahaemolyticus strains of a few specific serotypes, probably derived from a common clonal ancestor, have lately caused a pandemic of gastroenteritis. The organism is phylogenetically close to V cholerae, the causative agent of cholera.Methods The whole genome sequence of a clinical V parahaemolyticus strain RIMD2210633 was established by shotgun sequencing. The coding sequences were identified by use of Gambler and Glimmer programs. Comparative analysis with the V cholerae genome was undertaken with MUMmer.Findings The genome consisted of two circular chromosomes of 3 288 558 bp and 1877 212 bp; it contained 4832 genes. Comparison of the V parahaemolyticus genome with that of V cholerae showed many rearrangements within and between the two chromosomes. Genes for the type III secretion system (TTSS) were identified in the genome of V parahaemolyticus; V cholerae does not have these genes.Interpretation The TTSS is a central virulence factor of diarrhoea-causing bacteria such as shigella, salmonella, and enteropathogenic Escherichia coli, which cause gastroenteritis by invading or intimately interacting with intestinal epithelial cells. Our results suggest that V parahaemolyticus and V cholerae use distinct mechanisms to establish infection. This finding explains clinical features of V parahaemolyticus infections, which commonly include inflammatory diarrhoea and in some cases systemic manifestations such as septicaemia, distinct from those of V cholerae infections, which are generally associated with non-inflammatory diarrhoea.