In contrast, at days 14 and 28, epithelial cells were joined by complete apical junctional complexes and clearly showing an apically-basally polarized epithelia in both NP and control NM ALI cultures. On the other hand, we elected to focus on mucins MUC5AC and MUC5B because they are the two major components in the mucus of human airways, and lactoferrin. Despite not reaching statistical significance, we found that mucous and serous secretions were slightly increased in both cultures. The increased mucus production during mucociliary differentiation is probably due to the increased number of goblet cells, which were expressing both mucins in both cultures. These findings are partly in keeping with previous studies that have reported an increased mucin expression during differentiation of nasal epithelial cells in ALI culture. On the other hand, we also observed that MUC5B and lactoferrin secretions tended to be lower in NP compared to control NM ALI cultures. Since it has been described that submucosal glands and also certain antimicrobial proteins, most notably lactoferrin, are diminished in CRSwNP, our results for the MUC5B and lactoferrin secretions could be indicating that there is a glandular phenotype in control NM ALI cultures, that may be not well developed during the mucociliar differentiation of NP epithelial cells. Nevertheless, although we detected decreased levels of MUC5B and lactoferrin in NP compared to control NM, we are speculating because differences between both cultures did not reach statistical significance. Obviously, further studies are necessary to explore and confirm that epithelial cells have a glandular phenotype, or even if they are able to form glands, when cultured at the ALI system. In contrast to the similarities in mucociliary differentiation of both NP and control NM ALI cultures, we found relevant differences associated with inflammatory function of CRSwNP epithelium, when cytokine and chemokine production were analyzed in well-differentiated epithelium. Our findings are in keeping with previous studies that have reported the increase of pro-inflammatory cytokines, such as IL-8 and chemokines, as GM-CSF, eotaxin, and MCP1 in CRSwNP, compared to control nasal mucosa. These cytokines and chemokines have been implicated in eosinophil inflammation in nasal polyps and are downregulated with glucocorticoid or anti-leukotriene treatments. Furthermore, our results from apical washes, particularly those for IL-8 and GM-CSF, are in keeping with the literature describing increased levels of pro-inflammatory mediators in nasal lavages from CRSwNP patients compared to controls. The present study therefore provides direct evidence that fully differentiated epithelium obtained from NP epithelial cells may sustain an inflammatory function associated to CRSwNP by secreting higher levels of cytokines and chemokines than control NM epithelia. However, there are limitations to our study.