Abstract: To evaluate the toxic effects of cigarette smoke on human bronchial epithelial cells (BEAS-2B cells), the viability of BEAS-2B cells was detected with a cell counting kit (CCK-8) and the cell morphology was observed under an optical microscopy. Western Blot assay was conducted to detect the expression variations of extracellular-regulated protein kinases 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK1/2) and the phosphorylation level of p38. The release levels of inflammatory cytokines interleukin-(IL-)1β, IL-6 and IL-8 were detected by enzyme-linked immunosorbent assay. The results showed that:1) The viability of BEAS-2B cells significantly decreased after exposure to cigarette smoke. 2) Exposure to cigarette smoke activated the expression of phospho-(P-)ERK1/2, P-JNK1/2, P-p38 pathways and induced the release of inflammatory cytokines IL-1β, IL-6 and IL-8. 3) The release levels of inflammatory cytokines decreased significantly after ERK1/2, JNK1/2 and p38 pathways' being inhibited by specific inhibitors. In conclusion, the inflammation induced by cigarette smoke is regulated by mitogen-activated protein kinase (MAPK) pathways. These results provide a reference for the mechanism analysis of pulmonary inflammatory diseases induced by cigarette smoke.