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鞭毛功能在杀鲑气单胞菌致病性中具有独特作用,这与该细菌在水生环境中的运动性无关。

A unique role of flagellar function in Aliivibrio salmonicida pathogenicity not related to bacterial motility in aquatic environments.

作者信息

Nørstebø Simen Foyn, Paulshus Erik, Bjelland Ane Mohn, Sørum Henning

机构信息

Department of Food Safety and Infection Biology, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, PO Box 8146 Dep, 0033, Oslo, Norway.

出版信息

Microb Pathog. 2017 Aug;109:263-273. doi: 10.1016/j.micpath.2017.06.008. Epub 2017 Jun 7.

DOI:10.1016/j.micpath.2017.06.008
PMID:28602841
Abstract

Aliivibrio salmonicida is the causative agent of cold-water vibriosis, a septicemia of farmed salmonid fish. The mechanisms of disease are not well described, and few virulence factors have been identified. However, a requirement for motility in the pathogenesis has been reported. Al. salmonicida is motile by the means of lophotrichous polar flagella, consisting of multiple flagellin subunits that are expressed simultaneously. Here we show that flagellin subunit FlaA, but not FlaD, is of major importance for motility in Al. salmonicida. Deletion of flaA resulted in 62% reduction in motility, as well as a reduction in the fraction of flagellated cells and number of flagella per cell. Similarly, deletion of the gene encoding motor protein motA gave rise to an aflagellate phenotype and cessation of motility. Surprisingly, we found that Al. salmonicida does not require motility for invasion of Atlantic salmon. Nevertheless, in-frame deletion mutants defective of motA and flaA were less virulent in Atlantic salmon challenged by immersion, whereas an effect on virulence after i.p. challenge was only seen for the latter. Our results indicate a complex requirement for motility and/or flagellation in the pathogenesis of cold-water vibriosis, but the mechanisms involved remain unknown. We hypothesize that the differences in virulence observed after immersion and i.p. challenge are related to the immune response of the host.

摘要

杀鲑气单胞菌是冷水弧菌病的病原体,该病是养殖鲑科鱼类的一种败血症。疾病机制尚未得到充分描述,已鉴定出的毒力因子很少。然而,有报道称在发病机制中运动性是必需的。杀鲑气单胞菌通过丛生极鞭毛运动,丛生极鞭毛由多个同时表达的鞭毛蛋白亚基组成。在这里,我们表明鞭毛蛋白亚基FlaA而非FlaD对杀鲑气单胞菌的运动性至关重要。flaA的缺失导致运动性降低62%,同时有鞭毛的细胞比例和每个细胞的鞭毛数量也减少。同样,编码运动蛋白motA的基因缺失导致无鞭毛表型和运动停止。令人惊讶的是,我们发现杀鲑气单胞菌侵袭大西洋鲑不需要运动性。然而,motA和flaA的框内缺失突变体在通过浸泡攻击的大西洋鲑中致病性较低,而仅在后者中观察到腹腔注射攻击后对毒力的影响。我们的结果表明,在冷水弧菌病的发病机制中,对运动性和/或鞭毛形成有复杂的需求,但其中涉及的机制仍然未知。我们推测,浸泡和腹腔注射攻击后观察到的毒力差异与宿主的免疫反应有关。

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