Abstract
Streptococcus mutans (S. mutans) is the primary etiological agent of dental caries. The S. mutans enzyme sortase A (SrtA) is responsible for anchoring bacterial cell wall surface proteins involved in host cell attachment and biofilm formation. Thus, SrtA is an attractive target for inhibiting dental caries caused by S. mutans-associated acid fermentation. In this study, we observed that astilbin, a flavanone compound extracted from Rhizoma Smilacis Glabrae, has potent inhibitory activity against the S. mutans SrtA, with an IC50 of 7.5 μg/mL. In addition, astilbin was proven to reduce the formation of biofilm while without affecting the growth of S. mutans. The results of a molecular dynamics simulation and a mutation analysis revealed that the Arg213, Leu111, and Leu116 of SrtA are important for the interaction between SrtA and astilbin. The results of this study demonstrate the potential of using astilbin as a nonbactericidal agent to modulate pathogenicity of S. mutans by inhibiting the activity of SrtA.
Highlights
Dental caries is a common chronic disease that causes considerable anxiety, pain, tooth loss, malnutrition, and even disability across all age groups [1]
Many studies have shown that isogenic sortase A (SrtA) knockout strains exhibit a notable reduction in the ability to anchor surface proteins containing the canonical LPXTG motif, and are less lethal than wildtype strains in various animal models of infection [29,30]
The SrtA-mutants of S. mutans show a decreased ability to attach to human extracellular matrix proteins and to colonize the murine oral cavity and teeth [31]
Summary
Dental caries is a common chronic disease that causes considerable anxiety, pain, tooth loss, malnutrition, and even disability across all age groups [1]. The disease process mainly involves bacteria, including Streptococcus mutans, Streptococcus sanguis, Streptococcus sobrinus, Lactobacillus spp., and Streptococcus oralis [2,3]. Among these bacteria, the Gram-positive bacterium S. mutans is the primary etiological agent of human dental caries [4], while infecting cardiac endothelial cells and causing infective endocarditis [5]. In the absence of sucrose, the adhesion of S. mutans to the dental surface, or other bacteria in dental plaque, is mediated by several surface adhesins. One of the primary adhesins of S. mutans is streptococcal protein antigen P
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