Interleukin-33 induces mucin gene expression and goblet cell hyperplasia in human nasal epithelial cells

Distinct gene expression profiles and regulation networks of nasal polyps in eosinophilic and non‐eosinophilic chronic rhinosinusitis

“…According to recent interesting findings, an increase in poorly proliferated basal cells (p63+/Ki67+) was observed in the epithelium of nasal polyps, which resulted in an aberrant remodeled epithelium lacking proper barrier function . These morphological and functional changes in nasal epithelial cells may alter the local inflammatory environment since epithelial cell‐derived cytokines, such as IL33 and thymic stromal lymphopoietin (TSLP), were associated with and contributed directly to the pathophysiology of CRSwNP …”

Biologics in chronic rhinosinusitis with nasal polyposis

“…Interleukin-33 has emerged as a mediator that drives the pathogenesis of allergic disease, with data to suggest that it can exacerbate eosinophil-mediated airway inflammation, induce mucus production and goblet cell hyperplasia, and predispose to viral-induced asthma exacerbations. [60][61][62][63] In addition to its likely role in allergic asthma, increased expression of IL-33 messenger RNA and protein has been found in the sinus tissue of patients with CRSwNP compared with controls, 42 and elevated expression of ST2, the ligand-binding chain of the IL-33 receptor, was observed in sinus mucosa from CRSwNP compared with CRSsNP and healthy control subjects. 64 This alarmin may be of particular importance in AERD, as there is markedly increased epithelial expression of IL-33 in the nasal polyps of patients with AERD than in those from aspirin-tolerant CRSwNP patients, and in a mouse model of AERD, aspirin-induced reactions induce mast cell activation that is IL-33 dependent.…”

Birch pollen‐specific subcutaneous immunotherapy reduces ILC2 frequency but does not suppress IL‐33 in mice

“…Innate cytokines like IL‐33, TSLP and IL‐25 are known to be involved in mucus production and remodelling of the airways. Exposure of nasal epithelium to IL‐33 in vitro, results in an upregulated expression of the mucin gene, enhanced mucus production and goblet hyperplasia . This indicates that IL‐33 is sufficient to induce mucus production, even in the absence of other cells of the immune system, like ILC2s or Th2 cells.…”

“…Exposure of nasal epithelium to IL-33 in vitro, results in an upregulated expression of the mucin gene, enhanced mucus production and goblet hyperplasia. 30 This indicates that IL-33 is sufficient to induce mucus production, even in the absence of other cells of the immune system, like ILC2s or Th2 cells. This might explain why the mucus production after BP SCIT was not inhibited completely ( Figure 5 to suppress the increase in circulating ILC2s within the pollen season.…”