Correlation between CCL26 production by human bronchial epithelial cells and airway eosinophils: Involvement in patients with severe eosinophilic asthma

• Published in: Journal of allergy and clinical immunology 2015-10, Vol.136 (4), p.904-913
• Main Authors: Larose, Marie-Chantal, MSc, Chakir, Jamila, PhD, Archambault, Anne-Sophie, BSc, Joubert, Philippe, MD, Provost, Véronique, PhD, Laviolette, Michel, MD, Flamand, Nicolas, PhD
• Format: Article
• Language: English
• Subjects: Adult; Allergy and Immunology; Asthma; Asthma - immunology; Biopsy; Bronchi - pathology; bronchial epithelial cells; bronchial mucosa; CCL26; Cells, Cultured; chemokine; Chemokine CCL26; Chemokines; Chemokines, CC - metabolism; Disease Progression; Eosinophil Major Basic Protein - metabolism; Eosinophilia - immunology; eotaxin; Epithelial Cells - metabolism; Female; Gene expression; Humans; IL-13; Immunohistochemistry; inflammation; Interleukin-13 - immunology; Laboratories; Male; Recruitment; severe asthma; Values
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1016/j.jaci.2015.02.039

Background High pulmonary eosinophil counts are associated with asthma symptoms and severity. Bronchial epithelial cells (BECs) produce CC chemokines, notably CCL26 (eotaxin-3), which recruits and activates eosinophils from asthmatic patients. This suggests that CCL26 production by BECs might be involved in persistent eosinophilia in patients with severe asthma despite treatment with high corticosteroid doses. Objective We sought to determine whether CCL26 levels correlate with eosinophilia and asthma severity. Methods Human CC chemokine expression was assessed by means of quantitative PCR or a quantitative PCR array in vehicle- or IL-13–treated BECs. CCL26 was quantitated by means of ELISA. Immunohistochemistry analyses of CCL26 and major basic protein were done on bronchial biopsy specimens. Results IL-13 selectively induced CCL26 expression by BECs. This increase was time-dependent and more prominent in BECs from patients with severe eosinophilic asthma. CCL26 levels measured in supernatants of IL-13–stimulated BECs also increased with asthma severity as follows: patients with severe eosinophilic asthma > patients with mild asthma ≈ healthy subjects. Immunohistochemistry analyses of bronchial biopsy specimens confirmed increased levels of CCL26 in the epithelium of patients with mild and those with severe eosinophilic asthma. Tissue eosinophil counts did not correlate with CCL26 staining. However, sputum CCL26 levels significantly correlated with sputum eosinophil counts ( P