Abstract：
Arcobacter butzleri is a foodborne pathogen that mainly causes enteritis in humans, but the number of cases of bacteraemia has increased in recent years. However, there is still limited knowledge on the pathogenic mechanisms of this bacterium. To investigate how A. butzleri causes disease, single knockout mutants were constructed in the cadF, ABU_RS00335, ciaB, and flaAB genes, which might be involved in adhesion and invasion properties. These mutants and the isogenic wild-type (WT) were then tested for their ability to adhere and invade human Caco-2 and HT29-MTX cells. The adhesion and invasion of A. butzleri RM4018 strain was also visualized by a Leica CTR 6500 confocal microscope. The adhesion and invasion abilities of mutants lacking the invasion antigen CiaB or a functional flagellum were lower than those of the WTs. However, the extent of the decrease varied depending on the strain and/or cell line. Mutants lacking the fibronectin (FN)-binding protein CadF consistently exhibited reduced abilities, while the inactivation of the other studied FN-binding protein, ABU_RS00335, led to a reduction in only one of the two strains tested. Therefore, the ciaB and flaAB genes appear to be important for A. butzleri adhesion and invasion properties, while cadF appears to be indispensable.
摘要：
Butzleri杆菌是一种食源性病原体，主要引起人类肠炎，但是近年来菌血症的病例数量有所增加。然而,对这种细菌的致病机制的了解仍然有限。为了调查A.butzleri如何导致疾病，在cadF中构建单敲除突变体，ABU_RS00335,ciaB,和flaAB基因，这可能与粘附和侵入特性有关。然后测试这些突变体和等基因野生型(WT)粘附和侵入人Caco-2和HT29-MTX细胞的能力。还通过LeicaCTR6500共聚焦显微镜观察了牛乳杆菌RM4018菌株的粘附和侵袭。缺乏入侵抗原CiaB或功能性鞭毛的突变体的粘附和入侵能力低于WT。然而,降低的程度根据菌株和/或细胞系而变化。缺乏纤连蛋白（FN）结合蛋白CadF的突变体始终表现出降低的能力，而另一个研究的FN结合蛋白的失活，ABU_RS00335导致测试的两个菌株中的仅一个的减少。因此,ciaB和flaAB基因似乎对牛乳杆菌的粘附和侵袭特性很重要，而cadF似乎是不可或缺的。
