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.

<p>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.