Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model

Dietary obesity is regarded as a problem worldwide, and it has been revealed the strong linkage between obesity and allergic inflammation. Fatty acid-binding protein 5 (FABP5) is expressed in lung cells, such as alveolar epithelial cells (ECs) and alveolar macrophages, and plays an important role in...

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Autores principales: Kobayashi, Shuhei, Tayama, Shunichi, Phung, Hai The, Kagawa, Yoshiteru, Miyazaki, Hirofumi, Takahashi, Yu, Maruyama, Takashi, Ishii, Naoto, Owada, Yuji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538993/
https://www.ncbi.nlm.nih.gov/pubmed/33024217
http://dx.doi.org/10.1038/s41598-020-73935-y
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author Kobayashi, Shuhei
Tayama, Shunichi
Phung, Hai The
Kagawa, Yoshiteru
Miyazaki, Hirofumi
Takahashi, Yu
Maruyama, Takashi
Ishii, Naoto
Owada, Yuji
author_facet Kobayashi, Shuhei
Tayama, Shunichi
Phung, Hai The
Kagawa, Yoshiteru
Miyazaki, Hirofumi
Takahashi, Yu
Maruyama, Takashi
Ishii, Naoto
Owada, Yuji
author_sort Kobayashi, Shuhei
collection PubMed
description Dietary obesity is regarded as a problem worldwide, and it has been revealed the strong linkage between obesity and allergic inflammation. Fatty acid-binding protein 5 (FABP5) is expressed in lung cells, such as alveolar epithelial cells (ECs) and alveolar macrophages, and plays an important role in infectious lung inflammation. However, we do not know precise mechanisms on how lipid metabolic change in the lung affects allergic lung inflammation. In this study, we showed that Fabp5(−/−) mice exhibited a severe symptom of allergic lung inflammation. We sought to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the expression of FABP5 acts as a novel positive regulator of ST2 expression in alveolar ECs to generate retinoic acid (RA) and supports the synthesis of RA from type II alveolar ECs to suppress excessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation. Furthermore, high-fat diet (HFD)-fed mice exhibit the downregulation of FABP5 and ST2 expression in the lung tissue compared with normal diet (ND)-fed mice. These phenomena might be the reason why obese people are more susceptible to allergic lung inflammation. Thus, FABP5 is potentially a therapeutic target for treating ILC2-mediated allergic lung inflammation.
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spelling pubmed-75389932020-10-08 Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model Kobayashi, Shuhei Tayama, Shunichi Phung, Hai The Kagawa, Yoshiteru Miyazaki, Hirofumi Takahashi, Yu Maruyama, Takashi Ishii, Naoto Owada, Yuji Sci Rep Article Dietary obesity is regarded as a problem worldwide, and it has been revealed the strong linkage between obesity and allergic inflammation. Fatty acid-binding protein 5 (FABP5) is expressed in lung cells, such as alveolar epithelial cells (ECs) and alveolar macrophages, and plays an important role in infectious lung inflammation. However, we do not know precise mechanisms on how lipid metabolic change in the lung affects allergic lung inflammation. In this study, we showed that Fabp5(−/−) mice exhibited a severe symptom of allergic lung inflammation. We sought to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the expression of FABP5 acts as a novel positive regulator of ST2 expression in alveolar ECs to generate retinoic acid (RA) and supports the synthesis of RA from type II alveolar ECs to suppress excessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation. Furthermore, high-fat diet (HFD)-fed mice exhibit the downregulation of FABP5 and ST2 expression in the lung tissue compared with normal diet (ND)-fed mice. These phenomena might be the reason why obese people are more susceptible to allergic lung inflammation. Thus, FABP5 is potentially a therapeutic target for treating ILC2-mediated allergic lung inflammation. Nature Publishing Group UK 2020-10-06 /pmc/articles/PMC7538993/ /pubmed/33024217 http://dx.doi.org/10.1038/s41598-020-73935-y Text en © The Author(s) 2020 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Kobayashi, Shuhei
Tayama, Shunichi
Phung, Hai The
Kagawa, Yoshiteru
Miyazaki, Hirofumi
Takahashi, Yu
Maruyama, Takashi
Ishii, Naoto
Owada, Yuji
Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model
title Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model
title_full Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model
title_fullStr Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model
title_full_unstemmed Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model
title_short Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model
title_sort fatty acid-binding protein 5 limits ilc2-mediated allergic lung inflammation in a murine asthma model
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538993/
https://www.ncbi.nlm.nih.gov/pubmed/33024217
http://dx.doi.org/10.1038/s41598-020-73935-y
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