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High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation
PM(2.5) is particulate matter with a diameter of 2.5 μm or less. Airway macrophages are the key players regulating PM(2.5)-induced inflammation. High molecular weight hyaluronan (HMW-HA) has previously been shown to exert protective effects on PM(2.5)-induced acute lung injury and inflammation. Howe...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6539614/ https://www.ncbi.nlm.nih.gov/pubmed/31067702 http://dx.doi.org/10.3390/molecules24091766 |
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author | Shi, Qiwen Zhao, Lan Xu, Chenming Zhang, Leifang Zhao, Hang |
author_facet | Shi, Qiwen Zhao, Lan Xu, Chenming Zhang, Leifang Zhao, Hang |
author_sort | Shi, Qiwen |
collection | PubMed |
description | PM(2.5) is particulate matter with a diameter of 2.5 μm or less. Airway macrophages are the key players regulating PM(2.5)-induced inflammation. High molecular weight hyaluronan (HMW-HA) has previously been shown to exert protective effects on PM(2.5)-induced acute lung injury and inflammation. However, little is known about the detailed mechanism. In this study, we aimed to determine whether HMW-HA alleviates PM(2.5)-induced pulmonary inflammation by modulating macrophage polarization. The levels of M1 biomarkers TNF-α, IL-1β, IL-6, CXCL1, CXCL2, NOS2 and CD86, as well as M2 biomarkers IL-10, MRC1, and Arg-1 produced by macrophages were measured by ELISA, qPCR, and flow cytometry. In addition, the amount of M1 macrophages in lung tissues was examined by immunofluorescence of CD68 and NOS2. We observed a decline in PM(2.5)-induced M1 polarization both in macrophages and lung tissues when HMW-HA was administered simultaneously. Meanwhile, western blot analysis revealed that PM(2.5)-induced JNK and p38 phosphorylation was suppressed by HMW-HA. Furthermore, in vitro and in vivo studies showed that co-stimulation with HMW-HA and PM(2.5) promoted the expression and release of IL-10, but exhibited limited effects on the transcription of MRC1 and ARG1. In conclusion, our results demonstrated that HMW-HA ameliorates PM(2.5)-induced lung inflammation by repressing M1 polarization through JNK and p38 pathways and promoting the production of pro-resolving cytokine IL-10. |
format | Online Article Text |
id | pubmed-6539614 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-65396142019-05-31 High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation Shi, Qiwen Zhao, Lan Xu, Chenming Zhang, Leifang Zhao, Hang Molecules Article PM(2.5) is particulate matter with a diameter of 2.5 μm or less. Airway macrophages are the key players regulating PM(2.5)-induced inflammation. High molecular weight hyaluronan (HMW-HA) has previously been shown to exert protective effects on PM(2.5)-induced acute lung injury and inflammation. However, little is known about the detailed mechanism. In this study, we aimed to determine whether HMW-HA alleviates PM(2.5)-induced pulmonary inflammation by modulating macrophage polarization. The levels of M1 biomarkers TNF-α, IL-1β, IL-6, CXCL1, CXCL2, NOS2 and CD86, as well as M2 biomarkers IL-10, MRC1, and Arg-1 produced by macrophages were measured by ELISA, qPCR, and flow cytometry. In addition, the amount of M1 macrophages in lung tissues was examined by immunofluorescence of CD68 and NOS2. We observed a decline in PM(2.5)-induced M1 polarization both in macrophages and lung tissues when HMW-HA was administered simultaneously. Meanwhile, western blot analysis revealed that PM(2.5)-induced JNK and p38 phosphorylation was suppressed by HMW-HA. Furthermore, in vitro and in vivo studies showed that co-stimulation with HMW-HA and PM(2.5) promoted the expression and release of IL-10, but exhibited limited effects on the transcription of MRC1 and ARG1. In conclusion, our results demonstrated that HMW-HA ameliorates PM(2.5)-induced lung inflammation by repressing M1 polarization through JNK and p38 pathways and promoting the production of pro-resolving cytokine IL-10. MDPI 2019-05-07 /pmc/articles/PMC6539614/ /pubmed/31067702 http://dx.doi.org/10.3390/molecules24091766 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Shi, Qiwen Zhao, Lan Xu, Chenming Zhang, Leifang Zhao, Hang High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation |
title | High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation |
title_full | High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation |
title_fullStr | High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation |
title_full_unstemmed | High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation |
title_short | High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM(2.5)-Induced Lung Inflammation |
title_sort | high molecular weight hyaluronan suppresses macrophage m1 polarization and enhances il-10 production in pm(2.5)-induced lung inflammation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6539614/ https://www.ncbi.nlm.nih.gov/pubmed/31067702 http://dx.doi.org/10.3390/molecules24091766 |
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