With respect to gestational age, not only were the total levels of salivary IgA higher in FT (up to 2.5-fold) but also the complexity of IgA against bacterial species (Fig. 2A, Table 1), suggesting that prematurity can lead to a delay in IgA responses at initial stages of antigenic challenge. Longitudinal

comparisons of levels of IgA in PT and FT infants could be helpful to clarify the extent to which this difference is maintained over time. Previously, we suggested that patterns click here of specificity of IgA antibody responses to S. mutans antigens might be more important than total levels of reactive IgA antibodies. 15 In this study, we observed that patterns of protein bands reactive with salivary IgA were variable amongst newborn ( Fig. 2A). We reasoned that mucosal responses, most frequently detected in newborns to antigens of S. mitis, a pioneer colonizer of oral mucosa, might develop earlier than to S. mutans, which colonize children at a later age. 5, 13 and 14 By separating proteins in 6% SDS–PAGE gels it is possible to visualize the three main cell-associated antigens of S. mutans, Ag I/II, 21 GTF C 22 and GbpB 5 with molecular masses of 185, 160 and 56 kDa respectively. These antigens are involved in the capacity of S. mutans to adhere and accumulate in the dental biofilm. A previous study showed that some five-month-old

children presented with salivary IgA reactive to all this antigens, especially to GbpB and may have a role in modulating the level of colonization Pexidartinib order by S. mutans. 15 In the present study,

approximately 30% of the children evaluated (n = 16/48) presented IgA against AgI/II and GTFC, but not against GbpB ( Table 1). Also, 20% of saliva samples from newborn children were reactive with a S. mitis 202 kDa component ( Table 1), suggesting the presence of IgA reactive to IgA1-protease, an antigen important for S. mitis establishment in the oral cavity. 23 and 24 In the present study we analysed the specificity of salivary SIgA antibodies reactive with S. mutans, S. mitis and E. faecalis, to test whether SIgA antibodies reactive with commensal oral bacteria were induced by these bacteria and were, therefore, specific to them or Hydroxychloroquine in vivo whether they were induced by cross-reactions with other bacteria. The results of cross-adsorption showed that in half of the saliva tested (n = 5 of 10), there was a reduction of the salivary IgA to S. mutans when the plate was previously absorbed with S. mitis antigens. A similar result of levels of salivary IgA to S. mitis occurred when the plate was covered with S. mutans. The elimination of salivary IgA antibodies reactive with the test species following sequential adsorption of saliva samples with each streptococcal species supports partially the conclusion that the antibodies were cross-reactive rather than species specific, as described previously.