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, 2000; Ji et al., 2007). F. nucleatum induced Th3 (sIgA)- and Th1 (IFNc and IgG1)-mediated immune responses, whereas T. denticola induced a Th1 (IFNc and IgG1)-mediated response. This IFNc-mediated cytokine response was impaired Azastene in chronic periodontitis patients, and the Td92-induced IFNc levels were negatively associated with periodontal destruction in patients. These findings may provide new insights into the homeostatic interaction between the immune system and oral bacteria and the pathogenesis of periodontitis (Shin et al., 2013). P. micra (previously known as Peptostreptococcus) showed the strongest association with disease and was present at significantly higher absolute and relative numbers in the subgingival biofilm of periodontitis sites (Al-hebshi et al., 2014). There is an increasing amount of evidence on its role as a periodontal pathogen, along with other peptostreptococci (Rams et al., 1992; Kumar et al., 2005; Colombo et al., 2009; Belstrom et al., 2014). However, our study revealed that 88% of the sites of the periodontally healthy subjects expressed P. micra with a mean value of 105.5 bacteria, thus questioning selleck chemical the role of this bacterium in periodontal diseases. Moreover, our results led us to hypothesize that this bacterial species could be expressed in the interdental biofilm at higher levels than in the supragingival and subgingival biofilms of periodontally healthy subjects, although our conclusion is not certain because Uzel et al. (2011) used DNA�CDNA hybridization and we used real-time PCR to quantify the bacterial counts. The red complex, which is recognized as comprising the most important pathogens in adult periodontal disease (Suzuki et al., 2013), represents 8.08% of the 19 bacteria analyzed in the interdental biofilm. In accordance with the study by Griffen et al. (1998), P. gingivalis was detected in only 19% of healthy subjects. Our study reveals that P. gingivalis represents 0.02% of the interdental biofilm in healthy subjects, suggesting these subjects could develop CP-673451 molecular weight periodontal disease. Indeed, it has been shown that low levels of P. gingivalis (