?Fig.2.2. contamination. is considered to be pathogenic for dental caries, because of its ability to adhere Neu-2000 and accumulate in the dental biofilm in the presence of sucrose and to produce and tolerate high concentrations of acids, which promote tooth demineralization. Three main cell-associated antigens (Ags) of have been shown to be involved in the capacity of these microorganisms to adhere and accumulate in the dental biofilm. These antigens include an adhesin (AgI/II), glucosyltransferases (GTF) which synthesize glucan from sucrose, and glucan-binding protein B (GbpB) (21, 38, 39, 42). The biological role of these Ags in virulence has been demonstrated in animal models (3, 32, 35, 42) or in in vitro studies of biofilm formation (24). Several studies have also exhibited that induction of specific antibodies against each antigen can confer protection from dental caries development in animal models (16, 18, 39). The studies formed the basis for the use of these antigens in phase one clinical trials of caries Rabbit polyclonal to SZT2 vaccines in adults and older children (10, 36). Although can be detected in caries-free subjects, high proportions of these organisms in the dental biofilm are consistently associated with high caries activity (39). The earlier children become infected with seems to be associated with the eruption of primary molars, which normally takes place between 19 to 30 months of age. It is thought that these teeth provide noncolonized and retentive surfaces for biofilm formation (6). This period has been defined as a windows of infectivity because after about 30 months of age there is a decreasing risk for acquisition (6). It has been argued that this Neu-2000 reduced risk of contamination results from the establishment of a competitive commensal microbiota on tooth surfaces (6, 7). However, the influence of Neu-2000 the maturation of the host immune system on this process is usually unclear. Although high sucrose intake can promote heavy contamination associated with severe caries (40), differences in sucrose consumption do not usually result in different contamination levels and caries development. For example, within a high-sucrose-exposed populace of nursery children, we have observed a small subset of heavily infected Neu-2000 children from 24 to 30 months of age who did not develop the disease (23). In fact, in this subset, levels were often subsequently reduced during a 1-12 months follow-up period (23). High fluctuations in levels had also been observed in a populace at low risk for caries after 30 months of age (31). Variations in immunological status and the virulence of infecting genotypes may account for these observations. Previous studies have indicated a high diversity of patterns of salivary immunoglobulin A (IgA) response to Ags in children and adults (4, 5, 31). However, there has been no consistent evidence that differences in patterns of salivary IgA specificities or intensity of response influence the susceptibility to contamination and caries development. We hypothesize that the capacity to mount salivary IgA antibody responses to virulence-associated antigens early in life may influence the ability of to infect or to accumulate to significant levels in the oral cavity. To address this hypothesis, we have characterized the intensity and specificity of salivary IgA levels to antigens in a 1-12 months prospective study of 5- to 13-month-old children at high risk of contamination. Subjects were drawn from a populace with low socioeconomic status, high sucrose intake, and heavy exposure to (23, 27). Specific patterns of IgA antibody response to and antigens were compared between 21 matched pairs of children who were either infected or not infected at an early age with GbpB are associated with initial resistance to contamination in this populace. MATERIALS AND METHODS Study populace and design. The study populace included all the 5- to 13-month-old children who attended the 28 public nursery colleges in the city of Piracicaba, S?o Paulo, Brazil (Escolas Municipais de Ensino Infantil [EMEIs]). Thus, at.