Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.


The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Docosahexaenoic acid enhances amphiregulin-mediated bronchial epithelial cell repair processes following organic dust exposure.

Authors: Nordgren, Tara M; Heires, Art J; Bailey, Kristina L; Katafiasz, Dawn M; Toews, Myron L; Wichman, Christopher S; Romberger, Debra J

Published In Am J Physiol Lung Cell Mol Physiol, (2018 03 01)

Abstract: Injurious dust exposures in the agricultural workplace involve the release of inflammatory mediators and activation of epidermal growth factor receptor (EGFR) in the respiratory epithelium. Amphiregulin (AREG), an EGFR ligand, mediates tissue repair and wound healing in the lung epithelium. Omega-3 fatty acids such as docosahexaenoic acid (DHA) are also known modulators of repair and resolution of inflammatory injury. This study investigated how AREG, DHA, and EGFR modulate lung repair processes following dust-induced injury. Primary human bronchial epithelial (BEC) and BEAS-2B cells were treated with an aqueous extract of swine confinement facility dust (DE) in the presence of DHA and AREG or EGFR inhibitors. Mice were exposed to DE intranasally with or without EGFR inhibition and DHA. Using a decellularized lung scaffolding tissue repair model, BEC recolonization of human lung scaffolds was analyzed in the context of DE, DHA, and AREG treatments. Through these investigations, we identified an important role for AREG in mediating BEC repair processes. DE-induced AREG release from BEC, and DHA treatment following DE exposure, enhanced this release. Both DHA and AREG also enhanced BEC repair capacities and rescued DE-induced recellularization deficits. In vivo, DHA treatment enhanced AREG production following DE exposure, whereas EGFR inhibitor-treated mice exhibited reduced AREG in their lung homogenates. These data indicate a role for AREG in the process of tissue repair after inflammatory lung injury caused by environmental dust exposure and implicate a role for DHA in regulating AREG-mediated repair signaling in BEC.

PubMed ID: 29097425 Exiting the NIEHS site

MeSH Terms: Amphiregulin/metabolism*; Animals; Bronchi/cytology*; Bronchi/drug effects; Bronchi/metabolism; Docosahexaenoic Acids/pharmacology*; Dust/analysis*; Environmental Exposure/adverse effects*; Epithelial Cells/cytology*; Epithelial Cells/drug effects; Epithelial Cells/metabolism; ErbB Receptors/metabolism; Humans; Lung Injury/etiology; Lung Injury/metabolism; Lung Injury/pathology; Lung Injury/prevention & control*; Male; Mice; Mice, Inbred C57BL; Signal Transduction; Swine

to Top