Neither S. oralis nor A. naeslundii alone were found to form good biofilms, but growth in the two-species model resulted in abundant mutualistic growth [46]. AI-2 of S. oralis was recently found to be critical for such a mutualistic interaction [6]. Below and above the optimal concentration, mutualistic biofilm growth was suppressed. In S. mutans, LuxS was shown to be PF299 involved in biofilm formation and to affect the structure of biofilms [18, 22, 23], although its role in regulation of factors critical to bacterial adherence and biofilm formation is somewhat controversial. As shown previously, LuxS-deficiency significantly decreased brpA
expression, but no major differences were GSK3326595 price seen between wild-type and the LuxS-deficient mutants in expression of gtfBC, gbpB or spaP [18]. Similar results were also obtained by DNA microarray analysis in both planktonic [47] (Wen et al., unpublished data) and sessile populations (Wen et al., unpublished data). In a study using RealTime-PCR, however, Yoshida et al. [23] reported that transcription of gtfB and gtfC, but not gtfD, was up-regulated
in response to LuxS-deficiency. Like S. mutans and S. oralis, both S. sanguinis http://www.oralgen.lanl.gov and L. casei (Wen and Burne, unpublished data) possess LuxS. It remains unclear, however, whether LuxS in these bacteria is in fact involved AR-13324 chemical structure in cell-cell communication. Nevertheless, down regulation of luxS expression in S. mutans when grown in dual-species with L. casei and S. oralis would likely affect the absolute
concentration of AI-2 in the biofilms. Studies are ongoing to determine whether AI-2 signaling is functional between these bacterial species and whether alterations in luxS expression does in fact affect the expression of known virulence factors by S. mutans in mixed-species biofilms. It is well established that GtfB and GbpB are critical components of the sucrose-dependent pathway in S. mutans biofilm formation and cariogenicity. In the presence of sucrose, GtfB synthesizes copious Cell press α1,3-linked, water insoluble glucan polymers. Then, surface-associated glucan-binding protein GbpB and others bind to these polymers, facilitating intercellular adherence and biofilm accumulation by S. mutans. It would be expected that down-regulation of GtfB and GbpB would result in less biofilm formation. Surprisingly, our S. mutans-L. casei dual-species data showed that S. mutans accumulated more than 2-fold more biofilms while the expression of gtfB and gbpB was decreased. One possible explanation is that down regulation of GtfB and GbpB (and probably some other members of the Gtfs and Gbps) when grown together with L. casei altered the balance of glucans to glucan-binding proteins ratio or altered the glucan structure in a way that altered biofilm architecture. In fact, similar observations have also been reported recently by us and some other groups [11, 12, 48].
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