Procyanidin A2 Modulates IL-4-Induced CCL26 Production in Human Alveolar Epithelial Cells

• Published in: International journal of molecular sciences Vol. 17; no. 11; p. 1888
• Main Authors: Coleman, Sara L, Kruger, Marlena C, Sawyer, Gregory M, Hurst, Roger D
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 12.11.2016; MDPI
• Subjects: A549 Cells; airway inflammation; Airway management; Asthma; Asthma - drug therapy; Asthma - immunology; Catechin - pharmacology; Chemokine CCL26; Chemokines; Chemokines, CC - biosynthesis; Chemokines, CC - genetics; Drug Evaluation, Preclinical; eotaxin-3 (CCL26); Epithelial Cells - drug effects; Epithelial Cells - metabolism; Gene Expression; Humans; IFNγ; IL-4; Immunologic Factors - pharmacology; Inflammation; Interleukin-4 - physiology; Polyphenols; Proanthocyanidins - pharmacology; procyanidin A2; Pulmonary Alveoli - cytology; IFNγ; airway inflammation; IL-4; procyanidin A2; eotaxin-3 (CCL26)

Allergic asthma is an inflammatory lung disease that is partly sustained by the chemokine eotaxin-3 (CCL26), which extends eosinophil migration into tissues long after allergen exposure. Modulation of CCL26 could represent a means to mitigate airway inflammation. Here we evaluated procyanidin A2 as...