Other investigations have been done to confirm or refute these preliminary findings. It’s important to emphasize that the concentrations employed for each antigen was previously tested [6, 25, 29]. In this study, it was used 2.5 μg/mL of HmuY VX-765 in vivo versus 0.5 μg/mL of crude extract (5fold more of the recombinant protein). The capacity of only one molecule to induce a immune response is very low in comparison to a crude extract, which contains

AZD6244 research buy diverse somatic proteins and thus, can exposure many different epitopes to be recognized. Fas and Fas ligand are expressed in inflamed gingival tissue, as well as in the lymphocytes that accumulate in chronic periodontal lesions. The Fas-positive lymphocytes isolated from these lesions induce apoptosis by the anti-Fas antibody, which mimics the function of Fas ligand, while peripheral lymphocytes resist apoptosis under stimulation with this same antibody [30]. Thus, it has been suggested that the absence of Fas-mediated apoptosis in activated lymphocytes could contribute to chronic

disease and that exogenous Fas ligand may be a candidate for protection against the profile of chronic disease. In the present study, slightly elevated Fas expression by CD3+ T lymphocytes stimulated with P. gingivalis total antigens and HmuY was observed. The authors hypothesize that the lack of statistical significance in the results presented herein indicates that this may not be the primary

pathway that is being stimulated. Nonetheless, it is possible that the relatively small sample size employed herein was unable to produce demonstrable selleck compound Cyclin-dependent kinase 3 results with respect to Fas expression under the established experimental conditions. In addition, the present study showed that HmuY may also be an important stimulus used by P. gingivalis to induce increased expression of Bcl-2 in CD3+ T cells derived from CP patients. An inflammatory outcome is the most expected one following contact between host cells and P. gingivalis antigens, including HmuY, due to the association with necrotic cell death and membrane disruption, in addition to the exhibition of pro-inflammatory moieties. The absence or delay of apoptosis may play an important role in survival of PBMCs in CP patients and may even contribute to the chronicity of this disease. Further studies should be conducted to evaluate the receptor responding to the HmuY protein and identify the pathway involved in programmed cell death, as well as the role of HmuY in P. gingivalis infection in vivo. The P. gingivalis HmuY recombinant protein was also observed to inhibit Bcl-2 expression in PBMCs obtained from NP individuals, which was not the case in cells taken from CP patients. This protein is known to play an important in the “mounting” of host immune response by preventing apoptosis in lymphocytes.