First, some of our results may be have a low reproducibility due to we detected great variability, for instance, in the mucus and lactoferrin secretions. Moreover, the mucociliar differentiation of epithelial cells may varies between cultures from different donors, different wells, or even in different areas of the well. For instance, the presence of ciliated cells varies between different areas of the well. Secondly, we have not seen in the NP reconstituted epithelium the typical epithelial alterations of the sinus mucosa from patients with CRSwNP, where altered epithelium shows goblet or basal cell hyperplasia, or metaplasia. This could be due, at least in part, to the absence of inflammatory cells and the release of their inflammatory mediators in our ALI culture. Exposure of NP ALI cultures to inflammatory stimuli could potentially induce similar epithelial alterations as in the sinus mucosa of patients with CRSwNP. In fact, previous reports have demonstrated that in ALI cultures from normal human bronchial and guinea pig tracheal epithelial cells, induces goblet cell hyperplasia in culture. Nevertheless, to our knowledge, this is the first study demonstrating an elevated cytokine and chemokine secretion at basal level from NP reconstituted epithelia in ALI system. It could be relevant because provide more evidence that, as previously suggested by other studies, the 3D in vitro model of NP regenerated epithelium may be is a good model of the CRSwNP epithelium. Finally, future studies should investigate the proliferation, maintainenance, and differentiation of DNp63+ basal cells, which were identified in our study, and have been recently described as adult tissue stem cells of nasal epithelium. The biology and relevance of stem cells in nasal epithelium remain unclear. Identification of molecular mechanisms of nasal stem cells involved in repair, proliferation, and mucociliary differentiation under normal and pathological conditions, provides the potential for the development of new strategies for CRSwNP treatment. Sepsis is one of the most common causes of morbidity and mortality among admissions to the intensive care unit. Sepsis is a systemic dysregulated hyperinflammatory and/or antiinflammatory response to infectious stimuli, such as bacteria, viruses and fungi, which, when excessive, may progress to organ failure and death. Development of myocardial dysfunction is associated with increased morbidity and mortality of sepsis. More than 40% cases of sepsis have cardiovascular impairment and the presence of myocardial dysfunction can increase the mortality rate of affected patients to 70%. There is now good evidence that gender is a key determinant in the degree of the host inflammatory response and even of outcome in patients with sepsis. In a number of clinical and epidemiological studies, a significantly increased survival rate was reported in female patients when compared with male patients with sepsis.