Clara cell 10-kD protein in inflammatory upper airway diseases

Abstract

Purpose of review: To discuss the role of Clara cell 10-kD protein (CC10), an anti-inflammatory and immunomodulatory molecule, in inflammatory upper airway diseases, particularly in allergic rhinitis and chronic rhinosinusitis (CRS).

Recent findings: CC10 expression is downregulated in allergic rhinitis and CRS. CC10 can inhibit the expression of chitinase 3-like 1 protein and osteopontin in eosinophilic CRS and allergic rhinitis, respectively. CC10 can also suppress osteopontin-induced expression of Th2 and proinflammatory cytokines in airway epithelial cells, and CC10 gene transfection can inhibit NF-κB activity in airway epithelial cells. Proinflammatory and Th2 cytokines can diminish CC10 production, whereas Th1 cytokines and interleukin-10 can promote CC10 production in sinonasal mucosa. Allergen exposure leads to a transdifferentiation of CC10 secreting cells into trefoil factor family 1 secreting cells and/or goblet cells in upper airways, resulting in the diminished expression of CC10.

Summary: Allergen exposure and Th2 milieu can suppress the expression of CC10 in upper airways. CC10 can inhibit Th2-dominated eosinophilic inflammation in upper airways via multiple pathways.