Effects of Cigarette Smoke Extract on CXCL8 and CXCL1 Expression in oral Keratinocytes Induced by Synthetic Bacterial Lipoprotein Pam3CSK4

ABSTRACT Objective Cigarette smoking is associated with oral disease, whereas cigarette smoke extract (CSE) is an aqueous solution containing most of the compounds and toxins inhaled by smokers. Although it has been reported that CSE directly affected dysfunctions in examinations of various cell cultures, its effects on immune response to bacterial components in oral keratinocytes remain largely unknown. The present study investigated the effects of CSE on chemokine expression induced by Pam3CSK4 (Pam3), a mimic bacterial lipopeptide. Materials and Methods The effects of CSE on Pam3‐induced CXCL8/IL‐8 and CXCL1 expression in oral immortalized keratinocytes were examined using real‐time PCR and ELISA. Furthermore, western blotting was conducted to examine the effects of NF‐κB activated by Pam3 related to induction of CXCL8 and CXCL1 expression by CSE. Results CSE significantly decreased Pam3‐induced CXCL8 protein and CXCL1 mRNA expressions. In contrast, it showed no effects on expression of TLR1 or TLR2 mRNA following stimulation with Pam3. Preincubation with Bay 11‐7082, an inhibitor of NF‐κB, resulted in decreased CXCL8 and CXCL1 expressions induced by Pam3. Finally, CSE decreased NF‐κB activity induced by Pam3. Conclusions Cigarette smoking can modulate initial inflammatory responses induced by bacterial components in oral epithelium, thus contributing to reductions in the oral epithelial defense system during bacterial infection.