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The trimeric autotransporter adhesin BadA is required for in vitro biofilm formation by Bartonella henselae.
npj Biofilms and Microbiomes ( IF 7.8 ) Pub Date : 2019-03-14 , DOI: 10.1038/s41522-019-0083-8
Udoka Okaro 1 , Ryan Green 1 , Subhra Mohapatra 1 , Burt Anderson 1
Affiliation  

Bartonella henselae (Bh) is a Gram-negative rod transmitted to humans by a scratch from the common house cat. Infection of humans with Bh can result in a range of clinical diseases including lymphadenopathy observed in cat-scratch disease and more serious disease from persistent bacteremia. It is a common cause of blood-culture negative endocarditis as the bacterium is capable of growing as aggregates, and forming biofilms on infected native and prosthetic heart valves. The aggregative growth requires a trimeric autotransporter adhesin (TAA) called Bartonella adhesin A (BadA). TAAs are found in all Bartonella species and many other Gram-negative bacteria. Using Bh Houston-1, Bh Houston-1 ∆badA and Bh Houston-1 ∆badA/pNS2PTrcbadA (a partial complement of badA coding for a truncated protein of 741 amino acid residues), we analyze the role of BadA in adhesion and biofilm formation. We also investigate the role of environmental factors such as temperature on badA expression and biofilm formation. Real-time cell adhesion monitoring and electron microscopy show that Bh Houston-1 adheres and forms biofilm more efficiently than the Bh Houston-1 ∆badA. Deletion of the badA gene significantly decreases adhesion, the first step in biofilm formation in vitro, which is partially restored in Bh Houston-1 ∆badA/pNS2PTrcbadA. The biofilm formed by Bh Houston-1 includes polysaccharides, proteins, and DNA components and is susceptible to enzymatic degradation of these components. Furthermore, both pH and temperature influence both badA expression and biofilm formation. We conclude that BadA is required for optimal adhesion, agglutination and biofilm formation.



中文翻译:

三聚体自转运蛋白粘附素 BadA 是汉赛巴尔通体体外生物膜形成所必需的。

汉赛巴尔 通体( Bh ) 是一种革兰氏阴性杆菌,通过普通家猫的抓伤传播给人类。人类感染Bh可导致一系列临床疾病,包括猫抓病中观察到的淋巴结病以及持续性菌血症引起的更严重的疾病。它是血培养阴性心内膜炎的常见原因,因为细菌能够聚集生长,并在受感染的天然心脏瓣膜和人工心脏瓣膜上形成生物膜。聚集生长需要一种称为巴尔通体粘附素 A (BadA) 的三聚体自转运粘附素 (TAA)。TAA 存在于所有巴尔通体物种和许多其他革兰氏阴性细菌中。使用Bh Houston-1、Bh Houston-1 ΔbadABh Houston-1 ΔbadA /pNS2P Trc badA ( 741 个氨基酸残基的截短蛋白的badA编码的部分补充),我们分析了 BadA 在粘附和生物膜的形成。我们还研究了温度等环境因素对badA表达和生物膜形成的作用。实时细胞粘附监测和电子显微镜表明,Bh Houston-1 比Bh Houston-1 ΔbadA更有效地粘附和形成生物膜。badA基因的缺失显着降低了粘附,这是体外生物膜形成的第一步,在Bh Houston-1 ΔbadA /pNS2P Trc badA中部分恢复。Bh Houston-1形成的生物膜包含多糖、蛋白质和 DNA 成分,并且容易受到这些成分的酶促降解。此外,pH 值和温度都会影响badA表达和生物膜形成。我们得出结论,BadA 是最佳粘附、凝集和生物膜形成所必需的。

更新日期:2019-03-14
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