Curcumin suppresses Streptococcus mutans adherence to human tooth surfaces and extracellular matrix proteins.

Streptococcus mutans is the key causative agent of caries and infective endocarditis. The first step in biofilm development and the consequent initiation of further disease is bacterial adherence to host cell surfaces. Therefore, the aim of this study was to evaluate the inhibitory effect of curcumin on S. mutans adherence to extracellular matrices and tooth surfaces. The effect of curcumin on the ability of S. mutans to adhere to glass surfaces coated with collagen and fibronectin was tested in order to determine whether the decrease of the bacterial adhesion by curcumin is achieved by hindering the bacteria in adhering to collagen and/or fibronectin. Also, human teeth inoculated with S. mutans were treated with curcumin in vitro in order to assess the relevance of the anti-adhesive effect to oral conditions in vivo. The minimum inhibitory concentration (MIC) at which curcumin completely inhibited bacterial growth was 128 µg/mL. The addition of curcumin below the MIC diminished bacterial adherence onto both collagen- and fibronectin-coated glass surfaces and human tooth surfaces. It appears that the anti-adhesive effect of curcumin against S. mutans is mediated through collagen and fibronectin. These results support the widespread use of curcumin as a food-based antimicrobial agent.

Wnt and BMP signaling govern lineage segregation of melanocytes in the avian embryo.

Recent studies show that specification of some neural crest lineages occurs prior to or at the time of migration from the neural tube. We investigated what signaling events establish the melanocyte lineage, which has been shown to migrate from the trunk neural tube after the neuronal and glial lineages. Using in situ hybridization, we find that, although Wnts are expressed in the dorsal neural tube throughout the time when neural crest cells are migrating, the Wnt inhibitor cfrzb-1 is expressed in the neuronal and glial precursors and not in melanoblasts. This expression pattern suggests that Wnt signaling may be involved in specifying the melanocyte lineage. We further report that Wnt-3a-conditioned medium dramatically increases the number of pigment cells in quail neural crest cultures while decreasing the number of neurons and glial cells, without affecting proliferation. Conversely, BMP-4 is expressed in the dorsal neural tube throughout the time when neural crest cells are migrating, but is decreased coincident with the timing of melanoblast migration. This expression pattern suggests that BMP signaling may be involved in neural and glial cell differentiation or repression of melanogenesis. Purified BMP-4 reduces the number of pigment cells in culture while increasing the number of neurons and glial cells, also without affecting proliferation. Our data suggest that Wnt signaling specifies melanocytes at the expense of the neuronal and glial lineages, and further, that Wnt and BMP signaling have antagonistic functions in the specification of the trunk neural crest.

Effects of lithium on pigmentation in the embryonic zebrafish (Brachydanio rerio).

Pigment cell precursors of the embryonic zebrafish give rise to melanophores, xanthophores and/or iridophores. Cell signaling mechanisms related to the development of pigmentation remain obscure. In order to examine the mechanisms involved in pigment cell signaling, we treated zebrafish embryos with various activators and inhibitors of signaling pathways. Among those chemicals tested, LiCl and LiCl/forskolin had a stimulatory effect on pigmentation, most notable in the melanophore population. We propose that the inositol phosphate (IP) pathway, is involved in pigment pattern formation in zebrafish through its involvement in the: (1) differentiation/proliferation of melanophores; (2) dispersion of melanosomes; and/or (3) synthesis/deposition of melanin. To discern at what level pigmentation was being effected we: (1) counted the number of melanophores in control and experimental animals 5 days after treatment; (2) measured tyrosinase activity and melanin content; and (3) employed immunoblotting techniques with anti-tyrosine-related protein-2 and anti-melanocyte-specific gene-1 as melanophore-specific markers. Although gross pigmentation increased dramatically in LiCl- and LiCl/forskolin treated embryos, the effect on pigmentation was not due to an increase in the proliferation of melanophores, but was possibly through an increase in melanin synthesis and/or deposition. Collectively, results from these studies suggest the involvement of an IP-signaling pathway in the stimulation of pigmentation in embryonic zebrafish through the synthesis/deposition of melanin within the neural crest-derived melanophores.