Platelets enhance biofilm formation and resistance of endocarditis-inducing streptococci on the injured heart valve
Journal
The Journal of infectious diseases
Journal Volume
205
Journal Issue
7
Pages
1066
Date Issued
2012-04-01
Author(s)
Jung, Chiau-Jing
Yeh, Chiou-Yueh
Cheng, Hung-Wei
Lin, Chi-Shuan
Abstract
Infective endocarditis is a typical biofilm-associated infectious disease frequently caused by commensal streptococci, but the contribution of host factors in biofilm formation is unclear. We found that platelets are essential for in vitro biofilm formation by Streptococcus mutans or Streptococcus gordonii grown in human plasma. The biofilms were composed of bacterial floes embedded with platelet aggregates in layers, and a similar architecture was also detected in situ on the injured valves of a rat model of experimental endocarditis. Similar to planktonic cells, the streptococci in biofilms were also able to induce platelet aggregation, which facilitates multilayer biofilm formation. Entrapping of platelets directly enhances the resistance of streptococcal biofilms to clindamycin. Prophylactic antibiotics or aspirin can reduce but not prevent or abolish biofilm formation on injured heart valves. Therefore, the platelet is a host factor for commensal streptococci in the circulation to consolidate biofilm formation and protect bacteria against antibiotics.
SDGs
Other Subjects
acetylsalicylic acid; clindamycin; gentamicin; green fluorescent protein; immunoglobulin G; penicillin G; vancomycin; animal experiment; animal model; antibiotic resistance; article; bacterial endocarditis; bacterial strain; bacterium adherence; biofilm; commensal; controlled study; host pathogen interaction; human; human cell; in vitro study; in vivo study; minimum inhibitory concentration; nonhuman; pathogenesis; priority journal; rat; Streptococcus gordonii; Streptococcus mutans; thrombocyte aggregation; thrombocyte aggregation inhibition; valvular heart disease; Animals; Anti-Bacterial Agents; Anticoagulants; Aspirin; Biofilms; Blood Platelets; Clindamycin; Disease Models, Animal; Drug Resistance, Bacterial; Endocarditis; Heart Valves; Host-Pathogen Interactions; Human Experimentation; Humans; Rats; Streptococcal Infections; Streptococcus gordonii; Streptococcus mutans
Publisher
OXFORD UNIV PRESS INC
Type
journal article