However, this relationship changed dependent

upon the amount of periodontal disease and the amount of antibody to pathogens. Somewhat counterintuitively, in patients with more generalized periodontitis or having the highest level of antibody to the pathogens, the correlation in antibody levels to the pathogens and commensals were minimal. This finding supports the hypothesis that with chronic infection leading to oral tissue destruction, the host immune response Proteases inhibitor is dysregulated and selectively recognizes and responds to the pathogens, while not responding as robustly to the multitude of commensal bacteria within the context of the large polymicrobial ecology [7,30,37]. We did, however, observe a significant correlation between antibody levels to P. gingivalis and periodontal https://www.selleckchem.com/products/ferrostatin-1-fer-1.html status. These relationships were noted in blacks and males within this population of smoking patients and correlated specifically with the frequency of disease sites, linking the antibody more directly to the infectious challenge. In summary, the data show an elevated immune response to pathogens compared to commensals within this smoking population and suggesting that the host immune system has the ability to discriminate between potential pathogenic versus commensal species in the complex biofilms. Response to the pathogens was also shown to be greatest in the subjects with the greatest extent

of disease, comparable to previous findings in other populations and was most notable with antibody to P. gingivalis[21,38]. Meloxicam The observation that black males demonstrated the most severe periodontal disease, which was not commensurate with their level of smoking, supports the need for additional studies to identify the factor(s) that could be contributing to disease susceptibility/expression. While we acknowledge that this was not an exhaustive study of antibody specificities to oral bacterial, the findings highlight processes by which the immune system

recognizes pathogens such as P. gingivalis, and this response would be predicted to help to manage the periodontal disease immunopathology in adult populations. As importantly, it must be considered that antibodies are effector molecules in the host immune response and principal protective factors against extracellular bacterial pathogens. In that regard, previous studies have described antibody subclass distribution to oral pathogens [25,39,40] and suggested variations in the profiles related to the particular bacterial species. These findings were extended to potential success or failure of the antibodies to protect the host effectively. A range of studies have suggested that the immune response to oral pathogens does not mature effectively, as estimated via antibody avidity [41–46], and could contribute to lowered protective capacity. Furthermore, examination of the effector functions of antibodies to the oral pathogens has provided some challenge due to, for example, the gingipains from P.