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Updated: Oct 9, 2026
Microtiter Dish Biofilm Formation Assay
Published on: January 30, 2011
Expression of biofilm-associated genes in Staphylococcus aureus during storage of platelet concentrates
Meshari Alabdullatif1, Ahmed Alzahrani1
1Department of Pathology, College of Medicine, Imam Mohammad Ibn Saud Islamic University, Riyadh, Saudi Arabia.
Background And Objectives:
In transfusion medicine, the safety of platelet concentrates (PCs) is a major concern on account of contamination, mostly with Staphylococcus species. One of the most common contaminants is Staphylococcus aureus, which forms bacterial biofilms in PCs, posing a safety risk for transfusion patients. In this study, we investigate the contributions to biofilm formation of eno, ebps, and fib genes encoding surface proteins and of genes from the ica operon (icaA and icaD) encoding polysaccharide intercellular adhesin (PIA), along with their expression in bacteria grown in glucose-supplemented trypticase soy broth (TSBg) and PCs.
Materials And Methods:
Two strains of S. aureus (2039 and 2110) captured during routine PC screening were tested for biofilm formation in TSBg and under PC storage conditions, with mRNA collected at five time points and analyzed to determine expression of eno, ebps, fib, icaA, and icaD and their contributions to biofilm formation in both media.
Results:
In TSBg, S. aureus strain 2039 formed weak biofilms while 2110 formed strong. biofilms; however, in PCs, both strains formed strong biofilms. During biofilm formation, expression levels of icaA and icaD in both strains were generally significantly higher in TSBg than PCs. In contrast, expression of eno, ebps, and fib genes tended to be significantly higher under PC storage conditions.
Conclusion:
This study demonstrated that expression of genes involved in biofilm formation can be affected by growth media. Further investigation is needed to understand biofilm formation in the PC milieu and enhance transfusion safety.
Insights
Staphylococcus aureus biofilm formation in platelet concentrates (PCs) is influenced by growth conditions. Gene expression differs between standard broth and PC environments, impacting bacterial adhesion and transfusion safety.
Area of Science:
- Microbiology
- Transfusion Medicine
- Bacterial Pathogenesis
Background:
- Platelet concentrate (PC) contamination by Staphylococcus species, particularly Staphylococcus aureus, poses a significant risk in transfusion medicine.
- Staphylococcus aureus can form bacterial biofilms within PCs, further compromising transfusion safety.
- Understanding the genetic basis of biofilm formation is crucial for mitigating contamination risks.
Purpose of the Study:
- To investigate the role of specific genes (eno, ebps, fib, icaA, icaD) in Staphylococcus aureus biofilm formation.
- To analyze the expression patterns of these genes in bacteria grown in trypticase soy broth (TSBg) and platelet concentrates (PCs).
- To determine how different growth media affect biofilm formation and gene expression in Staphylococcus aureus.
Main Methods:
- Two strains of Staphylococcus aureus (2039 and 2110) isolated from PCs were used.
- Biofilm formation was assessed in glucose-supplemented trypticase soy broth (TSBg) and under PC storage conditions.
- Gene expression analysis of eno, ebps, fib, icaA, and icaD was performed at five time points using mRNA from bacteria in both media.
Main Results:
- Both S. aureus strains formed strong biofilms in PCs, whereas only strain 2110 formed strong biofilms in TSBg.
- Expression of icaA and icaD (involved in polysaccharide intercellular adhesin - PIA) was generally higher in TSBg compared to PCs.
- Expression of eno, ebps, and fib genes (encoding surface proteins) was generally higher under PC storage conditions.
Conclusions:
- Growth media significantly impacts the expression of genes involved in Staphylococcus aureus biofilm formation.
- The distinct gene expression profiles in PCs suggest a unique environment influencing bacterial adhesion.
- Further research is necessary to fully elucidate biofilm formation mechanisms in PCs and improve transfusion safety protocols.
