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Bacterial lipopolysaccharide (LPS) and interleukin (IL)-13 increase mucus secretion and inflammatory cytokine production in normal human bronchial epithelial (NHBE) cells. We evaluated the effect of club cell 10-kDa protein (CC10), an anti-inflammatory protein produced by epithelial cells, on mucus secretion, cell morphology and inflammatory cytokine production.  NHBE cells were cultured at an air–liquid interface with CC10 or vehicle and exposed to LPS on day 14. Mucin MUC5AC, IL-8 and granulocyte-macrophage colony-stimulating factor were measured in cell supernatants. MUC5AC and IL-8 mRNA expression were measured by real-time PCR. Western blotting was used to evaluate nuclear factor (NF)-κB and extracellular signal-regulated kinase (ERK) activation. Cells were evaluated histologically. Additionally, NHBE cells were exposed to IL-13 and CC10 for 14 days, and secretion of the mucins MUC5AC and MUC5B was measured.  MUC5AC secretion stimulated either by LPS or by IL-13 was attenuated by CC10 at 20 ng·mL −1  (p&lt;0.05). CC10 at 20 ng·mL −1  also attenuated IL-8 secretion (p&lt;0.05). MUC5AC and IL-8 mRNA expression were also decreased by CC10 (p&lt;0.05). CC10 attenuated phosphorylation of NF-κB (p&lt;0.05) and ERK1/2 (p&lt;0.05).  CC10 attenuates LPS-induced mucus secretion in airway cells, in part due to inhibition of NF-κB and ERK phosphorylation.

Club cell 10-kDa protein attenuates airway mucus hypersecretion and inflammation