Cargando…

Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma

Macrophage phenotype and function varies according to their polarized state, which in turn is dependent on microenvironmental stimuli. Under normal physiological conditions, lung interstitial macrophages that express interleukin (IL)-10 are considered to serve regulatory roles in the prevention of a...

Descripción completa

Detalles Bibliográficos
Autores principales: Nie, Hanxiang, Wang, Ailing, He, Qing, Yang, Qiaoyu, Liu, Linlin, Zhang, Guqin, Huang, Yi, Ding, Xuhong, Yu, Hongying, Hu, Suping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526127/
https://www.ncbi.nlm.nih.gov/pubmed/28810589
http://dx.doi.org/10.3892/etm.2017.4699
_version_ 1783252762038894592
author Nie, Hanxiang
Wang, Ailing
He, Qing
Yang, Qiaoyu
Liu, Linlin
Zhang, Guqin
Huang, Yi
Ding, Xuhong
Yu, Hongying
Hu, Suping
author_facet Nie, Hanxiang
Wang, Ailing
He, Qing
Yang, Qiaoyu
Liu, Linlin
Zhang, Guqin
Huang, Yi
Ding, Xuhong
Yu, Hongying
Hu, Suping
author_sort Nie, Hanxiang
collection PubMed
description Macrophage phenotype and function varies according to their polarized state, which in turn is dependent on microenvironmental stimuli. Under normal physiological conditions, lung interstitial macrophages that express interleukin (IL)-10 are considered to serve regulatory roles in the prevention of allergic reactions in the airways. However, the phenotypic profile of lung interstitial macrophages during the pathophysiology of asthma remains unknown. In the current study, the phenotypic characteristics of lung interstitial macrophages were investigated in an ovalbumin (OVA)-induced mouse model of asthma. The patterns of surface markers chemokine ligand and interleukin, and the metabolic enzyme activity of lung interstitial macrophages were investigated using flow cytometry analysis, reverse transcription-quantitative polymerase chain reaction, western blot analysis, and ELISA. It was observed that lung interstitial macrophages derived from OVA-induced asthmatic mice expressed phenotypic markers associated with alternatively activated macrophages (M2), including cluster of differentiation-206, transglutaminase 2, arginase (Arg) 1 and chemokine ligand (CCL)17/CCL22/CCL24 secretion. The M2 macrophages also exhibited increased levels of Arg1 activity and reduced levels of IL-10 expression, relative to macrophages derived from control mice. However, when evaluating the expression of markers associated with classically activated (M1) macrophages, namely inducible nitric oxide synthase and IL-12, it was observed that levels of M1 markers in the interstitial macrophages from asthmatic mice did not differ significantly to those in controls. Collectively, these data suggest that lung interstitial macrophages undergo a phenotypic switch from a regulatory macrophage phenotype under normal conditions to an alternative activation state in OVA-induced asthmatic mice.
format Online
Article
Text
id pubmed-5526127
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-55261272017-08-11 Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma Nie, Hanxiang Wang, Ailing He, Qing Yang, Qiaoyu Liu, Linlin Zhang, Guqin Huang, Yi Ding, Xuhong Yu, Hongying Hu, Suping Exp Ther Med Articles Macrophage phenotype and function varies according to their polarized state, which in turn is dependent on microenvironmental stimuli. Under normal physiological conditions, lung interstitial macrophages that express interleukin (IL)-10 are considered to serve regulatory roles in the prevention of allergic reactions in the airways. However, the phenotypic profile of lung interstitial macrophages during the pathophysiology of asthma remains unknown. In the current study, the phenotypic characteristics of lung interstitial macrophages were investigated in an ovalbumin (OVA)-induced mouse model of asthma. The patterns of surface markers chemokine ligand and interleukin, and the metabolic enzyme activity of lung interstitial macrophages were investigated using flow cytometry analysis, reverse transcription-quantitative polymerase chain reaction, western blot analysis, and ELISA. It was observed that lung interstitial macrophages derived from OVA-induced asthmatic mice expressed phenotypic markers associated with alternatively activated macrophages (M2), including cluster of differentiation-206, transglutaminase 2, arginase (Arg) 1 and chemokine ligand (CCL)17/CCL22/CCL24 secretion. The M2 macrophages also exhibited increased levels of Arg1 activity and reduced levels of IL-10 expression, relative to macrophages derived from control mice. However, when evaluating the expression of markers associated with classically activated (M1) macrophages, namely inducible nitric oxide synthase and IL-12, it was observed that levels of M1 markers in the interstitial macrophages from asthmatic mice did not differ significantly to those in controls. Collectively, these data suggest that lung interstitial macrophages undergo a phenotypic switch from a regulatory macrophage phenotype under normal conditions to an alternative activation state in OVA-induced asthmatic mice. D.A. Spandidos 2017-08 2017-06-28 /pmc/articles/PMC5526127/ /pubmed/28810589 http://dx.doi.org/10.3892/etm.2017.4699 Text en Copyright: © Nie et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Nie, Hanxiang
Wang, Ailing
He, Qing
Yang, Qiaoyu
Liu, Linlin
Zhang, Guqin
Huang, Yi
Ding, Xuhong
Yu, Hongying
Hu, Suping
Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
title Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
title_full Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
title_fullStr Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
title_full_unstemmed Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
title_short Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
title_sort phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526127/
https://www.ncbi.nlm.nih.gov/pubmed/28810589
http://dx.doi.org/10.3892/etm.2017.4699
work_keys_str_mv AT niehanxiang phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT wangailing phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT heqing phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT yangqiaoyu phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT liulinlin phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT zhangguqin phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT huangyi phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT dingxuhong phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT yuhongying phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma
AT husuping phenotypicswitchinlunginterstitialmacrophagepolarizationinanovalbumininducedmousemodelofasthma