The N3 subdomain in a domain of fibronectin-binding protein B isotype I is an independent risk determinant predictive for biofilm formation of Staphylococcus aureus clinical isolates

Abstract

Fibronectin-binding proteins (FnBP), FnBPA and FnBPB, are purported to be involved in biofilm formation of Staphylococcus aureus. This study was performed to find which of three consecutive N subdomains of the A domain in the FnBP is the key domain in FnBP. A total of 465 clinical isolates of S. aureus were examined for the biofilm forming capacity and the presence of N subdomains of FnBP. In the biofilm-positive strains, N2 and N3 subdomains of FnBPA, and N1 and N3 subdomains of FnBPB were significantly more prevalent. Multivariate logistic regression analysis of 246 biofilm-positive and 123 biofilm-negative strains identified only the FnBPB-N3 subdomain as an independent risk determinant predictive for biofilm-positive strains of S. aureus (Odds ratio [OR], 13.174; P<0.001). We also attempted to delete each of the fnbA-N2 and -N3 and fnbB-N1 and -N3 from S. aureus strain 8325-4 and examined the biofilm forming capacity in the derivative mutants. In agreement with the results of the multivariate regression analysis, deletion of either the fnbA-N2 or -N3, or fnbB-N1 did not significantly diminish the capacity of strain 8325-4 to develop a biofilm, while deletion of the fnbB-N3 did. Therefore, it is suggested that the FnBPB-N3 subdomain of isotype I may be a key domain in FnBP which is responsible for the causing biofilm formation in S. aureus clinical isolates.

Biofilm Formation and Its Relationship with the Molecular Characteristics of Food‐Related Methicillin‐Resistant Staphylococcus aureus (MRSA)

“…Biofilm‐negative isolates, on the other hand, belonged to SCC mec type V (Mirani and others ). Kwon and others () also supported this finding, and reported that MRSA strains with SCC mec type IV are more likely to form biofilm than other types of SCC mec . Other authors also reported that strong biofilm‐producing strains belong to SCC mec type IV and agr ‐type II; these authors suggested that SCC mec type IV and agr type II are a good combination for biofilm formation in foodborne MRSA isolates (Manago and others ; Cafiso and others ).…”

Reductive evolution of virulence repertoire to drive the divergence between community- and hospital-associated methicillin-resistant Staphylococcus aureus of the ST1 lineage

“…In fact, based on the scientific literature [37][38][39], it is reasonable to infer that the absence of genes encoding several enterotoxins, enterotoxin-likes, and the Panton-Valentine leucocidin in the genome of the vast majority of ST1-BR may have also reduced the cytotoxicity with an increase in the intracellular survival observed in this work. Indeed, the high tendency of low cytotoxic isolates to cause bacteremia has been previously demonstrated [39,41].…”

“…Global downregulation of proapoptotic exoproteins had previously been associated with decreased virulence and with an increase in S. aureus persistence [37][38][39]. However, the contribution of Spl proteases for S. aureus virulence is not clearly understood.…”

“…In fact, the correlation between cytotoxicity and intracellular survival in S. aureus has been well documented [37][38][39]46]. Some studies have already associated these properties with an improved ability of S. aureus to cause disseminated infections such as bloodstream infections (BSIs) [37,38]. Mutations in the global virulence regulators sarA and agr increase S. aureus intracellular survival and decrease bacterial cytotoxicity [37,39].…”

RpiRc regulates RsbU to modulate eDNA-dependent biofilm formation andin vivovirulence ofStaphylococcus aureusin a mouse model of catheter infection

“…SigB activity is tightly regulated by RsbU, leading to agr (RNAIII) inhibition and decreased extracellular proteases production, favoring FnBPs dependent biofilm formation (60, 61). The N3 sub-domain from the A domain of FnBPs is required for biofilm formation but not for fibronectin binding, meaning that binding to fibronectin and intercellular interaction during biofilm formation are independent (38, 62). Deletion of both genes is required for decreased biofilm formation and either fnbA or fnbB complementation alone restored MRSA biofilm amounts (38).…”