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. 2017 Aug 29;7:9565. doi: 10.1038/s41598-017-09869-9

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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13-S-HODE mediates steroid resistance via NF-κB and GR-α. Dietary lipids, absorbed through intestine are converted to long chain fatty acids which serve as a precursor for the formation of phospholipids. While, ω-6 fatty acids (red color phospholipid) are oxidized into pro-inflammatory lipid mediators, ω-3 is (green color phospholipid) oxidized to anti-inflammatory. 13-S-HODE is a lipid metabolite of linoleic acid (ω-6 fatty acid), oxidized by 15-lipoxygenase. 13-S-HODE, causes airway remodeling and goblet cell metaplasia by mitochondrial dysfunction via TRPV1 channels. In another independent pathway, it increases p-NFκB and reduces GR-α leading to steroid resistant asthma.