Scoffield Jessica A, Duan Dingyu, Zhu Fan, Wu Hui
Department of Pediatric Dentistry, School of Dentistry, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
State Key Laboratory of Oral Diseases, Department of Periodontology, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
PLoS Pathog. 2017 Apr 27;13(4):e1006300. doi: 10.1371/journal.ppat.1006300. eCollection 2017 Apr.
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.
铜绿假单胞菌会在囊性纤维化（CF）患者中引发严重的慢性肺部感染。尽管CF气道中存在多种交织在生物膜内的微生物，但许多研究仅关注铜绿假单胞菌发病机制在CF发病中的单一作用。最近，口腔共生链球菌已被鉴定为CF肺部的共居菌，但很少有研究探讨这些细菌在CF生物膜中所起的作用。我们研究了铜绿假单胞菌与口腔共生链球菌在双物种生物膜中的相互作用。在此我们报告，CF铜绿假单胞菌分离株FRD1可增强口腔共生副血链球菌对黑腹果蝇的生物膜形成和定殖。此外，铜绿假单胞菌胞外多糖藻酸盐的产生是促进副血链球菌生物膜形成和定殖所必需的。然而，在双物种生物膜中铜绿假单胞菌并未得到促进。此外，我们表明链球菌黏附素BapA1在体外介导了藻酸盐依赖性的副血链球菌生物膜增强，并且在存在FRD1的情况下，BapA1与另一种黏附素Fap1是副血链球菌体内定殖所必需的。综上所述，我们的研究突出了链球菌黏附素与铜绿假单胞菌藻酸盐之间的新关联，并揭示了副血链球菌潜在定殖于CF肺部并干扰铜绿假单胞菌发病机制的一种机制。
