Caspase-12 Silencing Attenuates Inhibitory Effects of Cigarette Smoke Extract on NOD1 Signaling and hBDs Expression in Human Oral Mucosal Epithelial Cells
Figure 11
Schematic depiction of the potential mechanism by which CSE-induced Caspase-12 activation dampens the defense response of oral mucosal epithelial cells to pathogenic microorganism through inhibition of the NOD1 signaling and hBDs production.
Mechanistically, CSE activated intracellular Caspase-12, which negatively regulated NOD1 signaling by suppressing NOD1 and NF-κB and inducing RIP2. As a part of downstream effectors of the signaling pathway, hBDs production was subsequently inhibited and the defense response to pathogens was dampened. CS: cigarette smoke; CSE: cigarette smoke extract.