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BioMed Research International
Volume 2015, Article ID 178369, 8 pages
Research Article

AT-RvD1 Modulates CCL-2 and CXCL-8 Production and NF-κB, STAT-6, SOCS1, and SOCS3 Expression on Bronchial Epithelial Cells Stimulated with IL-4

1Institute of Health Sciences, Department of Clinical Medicine, Laboratory of Experimental Immunopharmacology, Federal University of Triangulo Mineiro, Street Vigário Carlos 162, 38025-350 Uberaba, MG, Brazil
2Institute of Biological and Natural Sciences, Department of Genetics, Federal University of Triangulo Mineiro, Uberaba, MG, Brazil
3Institute of Health Sciences, Department of Clinical Medicine, Federal University of Triangulo Mineiro, Uberaba, MG, Brazil
4Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA

Received 15 July 2014; Revised 22 September 2014; Accepted 23 September 2014

Academic Editor: Carlo Jose Oliveira

Copyright © 2015 Jhony Robison de Oliveira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Bronchial epithelial cells represent the first line of defense against microorganisms and allergens in the airways and play an important role in chronic inflammatory processes such as asthma. In an experimental model, both RvD1 and AT-RvD1, lipid mediators of inflammation resolution, ameliorated some of the most important phenotypes of experimental asthma. Here, we extend these results and demonstrate the effect of AT-RvD1 on bronchial epithelial cells (BEAS-2B) stimulated with IL-4. AT-RvD1 (100 nM) decreased both CCL2 and CXCL-8 production, in part by decreasing STAT6 and NF-κB pathways. Furthermore, the effects of AT-RvD1 were ALX/FRP2 receptor dependent, as the antagonist of this receptor (BOC1) reversed the inhibition of these chemokines by AT-RvD1. In addition, AT-RvD1 decreased SOCS1 and increased SOCS3 expression, which play important roles in Th1 and Th17 modulation, respectively. In conclusion, AT-RvD1 demonstrated significant effects on the IL-4-induced activation of bronchial epithelial cells and consequently the potential to modulate neutrophilic and eosinophilic airway inflammation in asthma. Taken together, these findings identify AT-RvD1 as a potential proresolving therapeutic agent for allergic responses in the airways.