Objective: Nidus Vespae (NV) is the honeycomb of Polistes Olivaceous, P. Japonicus Saussure, and Parapolybiavaria Fabricius. Previously, we have shown the extract and chemical fractions from NV demonstrated remarkable capacities of inhibiting the acid production of oral bacteria at subminimum inhibitory concentration (MIC) concentrations. In searching the most potent anti-caries compounds in NV, we further separated the NV Chl/MeOH fraction and obtained two purified compounds: quercetin and kaemferol. The objective of this study was to assess the effectiveness of quercetin and kaemferol against S. mutans biofilm formation. Methods:The MIC, minimum biofilm inhibition concentration (MBIC 50 ) and minimum biofilm reduction concentration (MBRC 50 ) against Streptococcus mutans were examined for NV-derived of quercetin and kaemferol. The effectiveness of inhibiting S. mutans biofilm formation was further examined using in vitro biofilm model. Results:Both quercetin and kaemferol compounds demonstrated anti-biofilm activities when compared to the negative control. They are capable of reducing biofilm dry-weight, total protein, viable cells measured by colony forming unit (CFU), insoluble and soluble glucans formation. The in situ culture pH was less acidic when the biofilms were treated by quercetin and kaemferol. The quercetin and kaemferol demonstrated comparable capability of S. mutans killing in biofilms, compared to chlorhexidine.
Despite the cariogenic role of Candida suggested from recent studies, oral Candida acquisition in children at high risk for early childhood caries (ECC) and its association with cariogenic bacteria Streptococcus mutans remain unclear. Although ECC disproportionately afflicts socioeconomically disadvantaged and racial-minority children, microbiological studies focusing on the underserved group are scarce. Our prospective cohort study examined the oral colonization of Candida and S. mutans among 101 infants exclusively from a low-income and racial-minority background in the first year of life. The Cox hazard proportional model was fitted to assess factors associated with the time to event of the emergence of oral Candida and S. mutans. Oral Candida colonization started as early as 1 wk among 13% of infants, increased to 40% by 2 mo, escalated to 48% by 6 mo, and remained the same level until 12 mo. S. mutans in saliva was detected among 20% infants by 12 mo. The emergence of S. mutans by year 1 was 3.5 times higher (hazard ratio [HR], 3.5; confidence interval [CI], 1.1–11.3) in infants who had early colonization of oral Candida compared to those who were free of oral Candida ( P = 0.04) and 3 times higher (HR, 3.0; CI, 1.3–6.9) among infants whose mother had more than 3 decayed teeth ( P = 0.01), even after adjusting demographics, feeding, mother’s education, and employment status. Infants’ salivary S. mutans abundance was positively correlated with infants’ Candida albicans ( P < 0.01) and Candida krusei levels ( P < 0.05). Infants’ oral colonization of C. albicans was positively associated with mother’s oral C. albicans carriage and education ( P < 0.01) but negatively associated with mother’s employment status ( P = 0.01). Future studies are warranted to examine whether oral Candida modulates the oral bacterial community as a whole to become cariogenic during the onset and progression of ECC, which could lead to developing novel ECC predictive and preventive strategies from a fungal perspective.
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