Mohamed Jamal A, Teng Fang, Nallapareddy Sreedhar R, Murray Barbara E
Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical School, Houston 77030, USA.
J Infect Dis. 2006 Jan 15;193(2):231-40. doi: 10.1086/498871. Epub 2005 Dec 12.
We have shown previously that Enterococcus faecium SagA has broad-spectrum binding to extracellular matrix (ECM) proteins. In the present study, 2 sagA-like genes, salA and salB, were identified in Enterococcus faecalis.
We compared the salA and salB mutants; their parental strain, OG1RF; and the salB-complemented strain for binding to ECM proteins and biofilm formation.
The salB mutant (TX5123) grew more slowly but showed greater binding (approximately 10%-20% of cells bound) to fibronectin (FN) and collagen type I (CI) than did OG1RF (approximately 1% of cells bound) (P<.001). Although TX5123 showed decreased biofilm formation in tryptic soy broth plus 0.25% glucose (TSBG) (P<.001 vs. OG1RF), a marked increase in biofilm formation was shown by TX5123 but not by OG1RF when they were grown in TSBG plus horse serum (HS) or TSBG plus FN, and the increase was coincident with increased attachment and hydrophobicity of TX5123. Complementation of the salB mutant restored the wild-type phenotypes.
Whether SalB expression is ever sufficiently low in vivo to enhance adherence to ECM proteins or the serum-elicited increase in biofilm formation seen with the salB mutant in vitro is not currently known, but it is a potential way in which this organism could increase its adherence and biofilm formation during infection.
我们之前已经表明，粪肠球菌SagA与细胞外基质（ECM）蛋白具有广谱结合能力。在本研究中，在粪肠球菌中鉴定出了2个sagA样基因，即salA和salB。
我们比较了salA和salB突变体、它们的亲本菌株OG1RF以及salB互补菌株与ECM蛋白的结合情况和生物膜形成能力。
salB突变体（TX5123）生长较慢，但与纤连蛋白（FN）和I型胶原（CI）的结合能力（约10%-20%的细胞结合）比OG1RF（约1%的细胞结合）更强（P<0.001）。虽然TX5123在胰蛋白胨大豆肉汤加0.25%葡萄糖（TSBG）中生物膜形成减少（与OG1RF相比，P<0.001），但当TX5123和OG1RF在TSBG加马血清（HS）或TSBG加FN中生长时，TX5123的生物膜形成显著增加，而OG1RF没有，并且这种增加与TX5123的附着增加和疏水性增加相一致。salB突变体的互补恢复了野生型表型。
目前尚不清楚SalB在体内的表达是否会低到足以增强对ECM蛋白的粘附或体外观察到的salB突变体血清诱导的生物膜形成增加，但这是该生物体在感染期间增加其粘附和生物膜形成的一种潜在方式。
