A commensal streptococcus hijacks a Pseudomonas aeruginosa exopolysaccharide to promote biofilm formation

PLoS Pathogens

Jessica A. Scoffield¹  Dingyu Duan¹  Hui Wu¹  Fan Zhu² 

[1]Department of Pediatric Dentistry, School of Dentistry, University of Alabama at Birmingham, Birmingham, Alabama, United States of America

[2]State Key Laboratory of Oral Diseases, Department of Periodontology, West China Hospital of Stomatology, Sichuan University, Chengdu, China

关键词: Bacterial biofilms;    Pseudomonas aeruginosa;    Biofilms;    Streptococcus;    Drosophila melanogaster;    Cystic fibrosis;    Streptococcal infections;    Adhesins;   

DOI  :  10.1371/journal.ppat.1006300

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Pseudomonas aeruginosa causes devastating chronic pulmonary infections in cystic fibrosis (CF) patients. Although the CF airway is inhabited by diverse species of microorganisms interlaced within a biofilm, many studies focus on the sole contribution of P. aeruginosa pathogenesis in CF morbidity. More recently, oral commensal streptococci have been identified as cohabitants of the CF lung, but few studies have explored the role these bacteria play within the CF biofilm. We examined the interaction between P. aeruginosa and oral commensal streptococci within a dual species biofilm. Here we report that the CF P. aeruginosa isolate, FRD1, enhances biofilm formation and colonization of Drosophila melanogaster by the oral commensal Streptococcus parasanguinis. Moreover, production of the P. aeruginosa exopolysaccharide, alginate, is required for the promotion of S. parasanguinis biofilm formation and colonization. However, P. aeruginosa is not promoted in the dual species biofilm. Furthermore, we show that the streptococcal adhesin, BapA1, mediates alginate-dependent enhancement of the S. parasanguinis biofilm in vitro, and BapA1 along with another adhesin, Fap1, are required for the in vivo colonization of S. parasanguinis in the presence of FRD1. Taken together, our study highlights a new association between streptococcal adhesins and P. aeruginosa alginate, and reveals a mechanism by which S. parasanguinis potentially colonizes the CF lung and interferes with the pathogenesis of P. aeruginosa.

【 授权许可】

CC BY