Abstract
The principal etiological agent of human dental caries, Streptococcus mutans is a multi-virulent pathogen that can transform commensal oral microbial community to plaque biofilms. Major virulence factors that are associated with the cariogenicity of S. mutans include adhesion, acidogenicity and acidurity. All these pathogenic traits coordinate and alter the dental plaque ecology which provide room for interaction with other similar acidogenic and aciduric bacteria. This cariogenic flora increases the possibility of enamel demineralization which headway to caries development. The present study was aimed at evaluating the antimicrobial and antiinfective potential of a lichen secondary metabolite usnic acid (UA) against S. mutans. Minimum inhibitory concentration (MIC), Minimum bactericidal concentration (MBC) and growth kinetics were evaluated to determine the antimicrobial potential of UA against S. mutans. UA at 5 µg mL−1 and 10 µg mL−1 concentration were considered as MIC and MBC respectively. Effect on biofilm formation was microscopically assessed and found to be reduced in a concentration dependent manner. Gene expression of gtfB, gtfC, gtfD, vicR, ComDE and smu0630 was found to be downregulated upon treatment with sub-MIC of UA. Acidogenicity, acidurity, eDNA synthesis and response to oxidative stress were found to be attenuated by the influence of UA. It was also demonstrated to act on preformed mature biofilm of S. mutans. Moreover, UA was shown to possess very low frequency to acquire spontaneous resistance development in S. mutans. Besides, no morphological aberrations or toxic effect was instigated by UA in the human buccal epithelial cells as well as to the oral commensals. Altogether, these results demonstrate the therapeutic potential of usnic acid in the treatment of S. mutans infection.
Highlights
The principal etiological agent of human dental caries, Streptococcus mutans is a multi-virulent pathogen that can transform commensal oral microbial community to plaque biofilms
Whole genome of S. mutans has been sequenced completely from which existence of fourteen putative Twocomponent Regulatory Systems (TCRS) have been identified[10,11]. One among these TCRSs is the VicRK signal transduction system which regulates various physiological processes and virulence phenotypes of S. mutans including the expression of gtfBCD, biofilm formation, oxidative stress response, acid tolerance, bacteriocin production, genetic competence and cell d eath[12,13,14]
Lower concentration from 0.5 to 20 μg mL−1 was evaluated and found that at 5.0 μg mL−1 concentration of usnic acid (UA), visible inhibition in the growth of S. mutans was observed and the same concentration was considered as Minimum inhibitory concentration (MIC) (Fig. 1)
Summary
The principal etiological agent of human dental caries, Streptococcus mutans is a multi-virulent pathogen that can transform commensal oral microbial community to plaque biofilms. Whole genome of S. mutans has been sequenced completely from which existence of fourteen putative TCRSs have been identified[10,11] One among these TCRSs is the VicRK signal transduction system which regulates various physiological processes and virulence phenotypes of S. mutans including the expression of gtfBCD, biofilm formation, oxidative stress response, acid tolerance, bacteriocin production, genetic competence and cell d eath[12,13,14]. ComDE is another quorum-sensing signalling system that is essential for genetic competence and biofilm formation[15] These molecular circuits assist S. mutans to colonize on the tooth surface thereby altering the symbiotic oral ecosystem through shifting the non-pathogenic commensal flora to plaque microbiota which eventually progress the caries development[16]. Due to rapid increase in the incidence of antibiotic resistance, it is imperative to identify novel antimicrobial agents with potential to inhibit the various virulence aspects of S. mutans
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