Club cells, CC10 and self-control at the epithelial surface

Airway Epithelial Barrier Dysfunction in Chronic Obstructive Pulmonary Disease: Role of Cigarette Smoke Exposure

“…There are also barrier-protective mediators released by airway epithelial cells that may alter in response to cigarette smoke-induced barrier dysfunction (123). Club cell secretory protein-10 (CC10) acts as an essential barrier protective factor for airway epithelium (124). Downregulation of CC10 has been observed in lung tissue of patients with COPD and cigarette smoke-exposed animals, and may indirectly contribute to the leaky manifestation of airway epithelium (124)(125)(126)(127).…”

Club cells and CC16: another “smoking gun”? (With potential bullets against COPD)

“…CC16 polymorphism and local deficiency on the one hand, and a decreased number of club cells on the other hand, were reported as features of COPD [8,9], as confirmed by LAUCHO-CONTRERAS et al [10] in the current issue of the European Respiratory Journal. In previous studies, exogenous CC16 showed pharmacological properties that could decrease excess airway inflammation and mucus production in ex vivo models [11][12][13]. However, CC16 has not demonstrated physiological properties, as shown in a prior report on CC16-deficient mice, which were not more susceptible to changes induced by cigarette smoke [14].…”

Club Cells, Their Secretory Protein, and COPD

“…Th ey have been ascribed several protective roles, including airway repair aft er injury, secretion of antiinfl ammatory and immunomodulatory proteins, and detoxifi cation. 1 Th e study by Gamez et al 2 in this issue of CHEST (see page 1467 ) reports a reduction in the number of club cells in bronchial biopsy specimens from patients with COPD compared with matched normal smokers, suggesting that these cells may normally have a protective role against the development of airway obstruction. Ablation of club cells in transgenic mice results in squamous metaplasia of the airways with impaired epithelial cell regeneration and peribronchiolar fi brosis reminiscent of the changes seen in COPD airways.…”

“…Mortality, hospital lengths of stay, and health-care costs are typically greater among patients with respiratory failure complicated by VAP compared with patients who do not develop VAP. 1 Moreover, we know that the administration of inappropriate initial antibiotic therapy for VAP, usually due to the presence of multidrug-resistant bacteria as the causative pathogens, is associated with greater hospital mortality and longer hospital lengths of stay. 2 Th ese outcome-infl uencing characteristics of VAP make it an important infection for intensivists to manage in an optimal manner.…”