The bronchial epithelium covers the surface of the proximal airways and represents a barrier between inhaled air and the bronchial submucosa. The epithelium function as a protective barrier depends upon the mucociliary system which traps and eliminates from the airways the toxic particules and materials inhaled, and upon the intercellular junctions which prevent the diffusion within the epithelium of inhaled contaminants failed to be trapped by the mucus. Nicotinic receptors, present in the bronchial epithelium, bind endogenous acetylcholine or inhaled nicotine but their role are still discussed, while the α7 receptor in the skin seems to play a key role in the keratinocyte differentiation. We have observed that α3, α5 and β2-subunits of nicotinic receptors are expressed during the fetal development precisely when intercellular junctions appear. In vitro, the expression of α3, α5 and β2-subunits is associated with ciliary cell differentiation. At last, the in vitro inactivation of nicotinic receptors by mecamylamine, a reversible antagonist, decreases E cadherin and connexine 43 in the intercellular spaces, transepithelial resistance and the functionality of gap junctions. These results suggest that nicotinic receptors are involved in the development and maintenance of the epithelium cohesion.