Background: Cigarette smoke and interleukin-17A (IL-17A) are involved in inflammatory airway diseases, and the mechanisms behind these processes are still poorly understood. We investigated if recombinant human IL-17A in combination with cigarette smoke extract (CSE) increases the level of inflammatory cytokine and if CSE has effect on the expression of IL-17A receptor in normal human bronchial epithelial cells. Methods: BEAS-2B cells were used. IL-8 mRNA expression was determined by real-time PCR and released IL-8 in culture supernatant was measured by ELISA. IL-17 receptor A (IL-17RA) and IL-17RC expressions were evaluated by real-time PCR, Western blot analysis, or FACS. Results: IL-17A increased IL-8 transcripts and the release of IL-8 in a dose-dependent manner. CSE treatment significantly enhanced IL-17A-mediated IL-8 production. CSE induced both IL-17RA and IL-17RC mRNA expression and increased protein expression of both receptors in total cellular lysates. CSE up-regulated the expression of surface membrane IL-17RA. Conclusions: CSE enhances IL-17A-induced IL-8 production. Increased IL-17RA and IL-17RC by CSE might contribute to this enhanced inflammatory response.