Title 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
Author An Sung Kwon1, Dong Hoon Lim2, Hyo Jung Shin1, Geon Park3, Jong H. Reu1, Hyo Jin Park1, Jungmin Kim4*, and Yong Lim1*
Address 1Department of Microbiology, Medical School, Chosun University, Gwangju 501-759, Republic of Korea, 2Department of Urology, Medical School, Chosun University, Gwangju 501-759, Republic of Korea, 3Department of Laboratory Medicine, Medical School, Chosun University, Gwangju 501-759, Republic of Korea , 4Department of Microbiology, Kyungpook National University, School of Medicine, Daegu 700-422, Republic of Korea
Bibliography Journal of Microbiology, 51(4),499-505, 2013,
DOI 10.1007/s12275-013-3319-y
Key Words fibronectin-binding proteins, N3 subdomains of FnBPB, biofilm, S. aureus
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.