The respiratory epithelium of the upper airways is a first‐line defence against inhaled irritants, pathogens and allergens. It ensures a physical barrier provided by apical junctions and mucociliary clearance to avoid excessive activation of the immune system. The epithelium also forms a chemical and immunological barrier, extensively equipped to protect the airways against external aggressions before the adaptive immune system is required. Under normal circumstances, the epithelium is capable of recovering rapidly after damage. This manuscript reviews these main properties of the upper airway epithelium as well as its reported impairments in chronic inflammatory diseases. The knowledge on normal epithelial functions and their dysregulation in upper airway diseases should help to design new epithelial‐targeted treatments.

Background In Belgium, COVID-19 epidemy began on February 4, 2020 with a peak on April 10, 2020. Patients with cystic fibrosis (CF) followed in the Cliniques universitaires Saint-Luc were rapidly isolated before the government lockdown. Methods After the peak of the epidemy, we measured anti-SARS-CoV-2 IgM and IgG antibodies in 149 patients and collected clinical data. Results Only 3 asymptomatic patients presented IgG against the virus. In one patient hospitalized for COVID-19 (positive molecular testing), we did not detect any anti-SARS-CoV-2 antibodies, as in thirty-five other symptomatic patients considered as possible cases. Conclusions Even if respiratory symptoms linked to CF are frequent and compatible with COVID-19, anti-SARS-CoV-2 IgG antibodies were detected only in 3 asymptomatic patients. This reassuring study concerning the risk of COVID-19 in patients with CF illustrates the difficulty to distinguish COVID-19 symptoms from respiratory exacerbations and the need of generalized molecular testing to make a precise diagnosis.

BackgroundChronic obstructive pulmonary disease (COPD) is a devastating lung disease, representing the third cause of mortality worldwide. In COPD, the bronchial epithelium displays several structural and functional abnormalities involving barrier integrity, polarity, cell differentiation and epithelial-to-mesenchymal transition, as well as inflammation. Although COPD is currently considered as an irreversible disease, the (ir)reversible nature of those changes ex vivo remains poorly known.MethodsThe persistence of COPD epithelial features was assessed in very long-term (10 weeks) primary cultures of air/liquid interface (ALI)-reconstituted airway epithelium from non-smoker controls, smoker controls, and COPD patients. The role of inflammation in promoting this phenotype was also explored by stimulating ALI cultures with a cytokine mix of TNF-α, IL-6 and IL-1β.ResultsAlmost all epithelial defects (barrier dysfunction, impaired polarity, lineage abnormalities) observed in smokers and COPD persisted in vitro up to week 10, except IL-8 release and epithelial-to-mesenchymal transition which declined over time. Cytokine treatment induced COPD-like changes and was able to reactivate epithelial-to-mesenchymal transition in COPD cells.ConclusionsThe airway epithelium from smokers and COPD patients displays a memory of its native state and previous injuries by cigarette smoking, which is multidimensional and sustained for years, therefore probably residing in basal stem cells.

This report highlights the usefulness of bronchoscopy in case of recurrent pneumonia with the same localization even in CF patients where the presence of bronchiectasis as promoting factor of infections could delay the diagnosis.