d by bacteria in the placental microbiome [17]. The placental microbiome is quite equivalent for the human oral microbiome as well as the full-term neonatal gut microbiome; colonised largely by Actinobacteria, Proteobacteria, Bacteroidetes and Firmicutes. Post-natally, the exposure of the infant towards the mother’s skin microbiota throughout breastfeeding also influences the gut microbiota. Thus the variety of oral microbial species that the infant is exposed to orally, and any subsequent choice amongst these species, determines the establishment on the gut microbiome [16]. Only one particular group of workers have studied salivary nucleotide metabolites, reporting low concentrations (1 M) of inosine, xanthine and hypoxanthine in adult saliva [18]. In plasma, nucleotide metabolite concentrations are usually significantly less than 1 M, together with the exception of uric acid and uridine [19,20]. We confirmed these residual levels of purine/pyrimidine nucleosides and bases in adult saliva, though many adults exhibited salivary patterns that carried echoes of the neonatal pattern�a variance that might arise from genetic polymorphism within the population, one example is, of nucleoside transporters. We demonstrated that the neonatal salivary STF62247 pattern evolved into the adult pattern more than a period among six weeks and six months, with an apparent distinction amongst purines and pyrimidines. Such an early transition was unexpected but in retrospect this seems to confirm a hyperlink involving the neonatal pattern and weaning.
Effect of H2O2 on bacterial growth. The effect of growing H2O2 concentration (000 M) on bacterial growth. Hydrogen peroxide was added to nutrient broth inoculated with bacteria and incubated for 24 h at 37, except for L. plantarum, which was incubated for 48 h. The concentration of cells was determined as turbidity by measuring absorbance at 600 nm. Values represent the meanD (n = 3).
Salivary nucleotide metabolites and XO regulate 
bacterial development. Bacteria have been incubated with breast milk and simulated neonatal saliva for 24 h at 37 and after that enumerated by sub-culturing onto agar plates. Values represent 20072125 the meanD (n = 3). (A) Bactericidal effects of H2O2 generated by breastmilk (XO) and growing concentrations of salivary xanthine and hypoxanthine (00 M). Figure displays the concentration-dependent impact of xanthine and hypoxanthine versus log CFU/mL. ANOVA was utilised to compare among multiple means. (B) The impact of breastmilk plus simulated neonatal saliva (with and devoid of supplements) on bacterial counts (CFU/mL). Bacteria had been incubated with breastmilk and saliva alone (Control), or supplemented with nucleotide metabolites omitting xanthine/hypoxanthine (Full supplement except X&HX), or the latter with xanthine/hypoxanthine (Full supplement), or the latter with oxypurinol (Complete supplement + Oxypurinol) (see Table 2). Means have been compared by t-test: p0.05; p0.01; ns, not significant.
We could exclude dental flora, pathological conditions and neonatal stress as the cause of raised salivary metabolite concentrations in neonates, which suggests that specific transport mechanisms may possibly be active inside the salivary glands of neonates. We have pointed out that salivary hypoxanthine and xanthine can stimulate peroxide production via XO, therefore activating the `LPO system’. Other salivary nucleosides and bases can be readily utilised by the nucleotide salvage pathways in heterotrophic oral bacteria [1], or when nucleosides/bases are swallowed in
Table 2. Supplemented saliva. Four ‘simulated ne