Staphylococcus aureus is a major cause of hospital-associated infections worldwide. The
organism’s ability to form biofilms has led to resistance against current treatment options
such as beta-lactams, glycopeptides, and daptomycin. The ArlRS two-component system
is a crucial regulatory system necessary for S. aureus autolysis, biofilm formation, capsule
synthesis, and virulence. This study aims to investigate the role of the arlR deletion mutant
in the detection and activation of S. aureus. We created an arlR deleted mutant and complementary
strains and characterized their impact on the strains using partial growth measurement.
The quantitative real-time PCR was performed to determine the expression of
icaA, and the microscopic images of adherent cells were captured at the optical density of
600 to determine the primary bacterial adhesion. The biofilm formation assay was utilized
to investigate the number of adherent cells using crystal violet staining. Eventually, the
Triton X-100 autolysis assay was used to determine the influence of arlR on the cell autolytic
activities. Our findings indicate that the deletion of arlR reduced the transcriptional
expression of icaA but not icaR in the ica operon, leading to decrease in polysaccharide
intercellular adhesin (PIA) synthesis. Compared to the wild-type and the complementary
mutants, the arlR mutant exhibited decreased in biofilm production but increased autolysis.
It concluded that the S. aureus response regulatory ArlR influences biofilm formation,
agglutination, and autolysis. This work has significantly expanded our knowledge of the
ArlRS two-component regulatory system and could aid in the development of novel antimicrobial
strategies against S. aureus. |
