Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness

We have shown in the past studies that fine particulate matter (PM2.5) exposure increases airway hyperresponsiveness and leads to lung inflammation damage. Interleukin (IL)-37 plays a inhibitory role in inflammation activation and maintenance. However, the function of IL-37 in the above processes ke...

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Autores principales:	Min Wang, Shujie Hou, Xi Lu, Jingwen Li, Rongqin Li, Xixin Yan
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	interleukin (IL)-37 fine particulate matter (PM2.5) airway hyperresponsiveness human airway smooth muscle cells, IL-1R8 Environmental pollution TD172-193.5 Environmental sciences GE1-350
Acceso en línea:	https://doaj.org/article/99f1b91132d34ff8bf0bef94fe87b8d0
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spelling	oai:doaj.org-article:99f1b91132d34ff8bf0bef94fe87b8d02021-11-06T04:15:06ZInterleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness0147-651310.1016/j.ecoenv.2021.112890https://doaj.org/article/99f1b91132d34ff8bf0bef94fe87b8d02021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321010022https://doaj.org/toc/0147-6513We have shown in the past studies that fine particulate matter (PM2.5) exposure increases airway hyperresponsiveness and leads to lung inflammation damage. Interleukin (IL)-37 plays a inhibitory role in inflammation activation and maintenance. However, the function of IL-37 in the above processes keep unclear. We aim to explore the role of IL-37 in PM2.5-induced airway hyperresponsiveness in this study. A nose-only PM2.5 online concentration, enrichment and exposure instrument was also applied to generate mice model of airway hyperresponsiveness. A transgenic mice strain using a CMV promoter to express human IL-37b (hIL-37tg) was obtained. PM2.5 exposure was shown to increase airway resistance, followed by lung inflammation and IL-1β, TNFα, and IL-6 release, which was inhibited by IL-37tg mice and mice administrated recombinant human IL-37 intranasally (i.n). Moreover, expression of the proliferation-related protein PCNA and migration-related proteins MMP-2, MMP-9, and Vimentin was reduced in lung tissues of IL-37tg mice and mice given recombinant human IL-37 i.n. Abnormal cell contraction, proliferation, and migration of human airway smooth muscle cells (hASMCs) incubated with PM2.5 were also decreased by IL-37 treatment. In addition, IL-37 intervention of hASMCs before PM2.5 incubation decreased cytoplasmic calcium level and expression of PCNA, MMP-2, MMP-9 and Vimentin. Finally, knockdown of the IL-37 receptor IL-1R8 gene eliminated the protective effects of IL-37 in the above responses. We conclude that IL-37 inhibits inflammation activation and disease severity of airway hyperreactivity by PM2.5 induction.Min WangShujie HouXi LuJingwen LiRongqin LiXixin YanElsevierarticleinterleukin (IL)-37fine particulate matter (PM2.5)airway hyperresponsivenesshuman airway smooth muscle cells, IL-1R8Environmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 227, Iss , Pp 112890- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	interleukin (IL)-37 fine particulate matter (PM2.5) airway hyperresponsiveness human airway smooth muscle cells, IL-1R8 Environmental pollution TD172-193.5 Environmental sciences GE1-350
spellingShingle	interleukin (IL)-37 fine particulate matter (PM2.5) airway hyperresponsiveness human airway smooth muscle cells, IL-1R8 Environmental pollution TD172-193.5 Environmental sciences GE1-350 Min Wang Shujie Hou Xi Lu Jingwen Li Rongqin Li Xixin Yan Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness
description	We have shown in the past studies that fine particulate matter (PM2.5) exposure increases airway hyperresponsiveness and leads to lung inflammation damage. Interleukin (IL)-37 plays a inhibitory role in inflammation activation and maintenance. However, the function of IL-37 in the above processes keep unclear. We aim to explore the role of IL-37 in PM2.5-induced airway hyperresponsiveness in this study. A nose-only PM2.5 online concentration, enrichment and exposure instrument was also applied to generate mice model of airway hyperresponsiveness. A transgenic mice strain using a CMV promoter to express human IL-37b (hIL-37tg) was obtained. PM2.5 exposure was shown to increase airway resistance, followed by lung inflammation and IL-1β, TNFα, and IL-6 release, which was inhibited by IL-37tg mice and mice administrated recombinant human IL-37 intranasally (i.n). Moreover, expression of the proliferation-related protein PCNA and migration-related proteins MMP-2, MMP-9, and Vimentin was reduced in lung tissues of IL-37tg mice and mice given recombinant human IL-37 i.n. Abnormal cell contraction, proliferation, and migration of human airway smooth muscle cells (hASMCs) incubated with PM2.5 were also decreased by IL-37 treatment. In addition, IL-37 intervention of hASMCs before PM2.5 incubation decreased cytoplasmic calcium level and expression of PCNA, MMP-2, MMP-9 and Vimentin. Finally, knockdown of the IL-37 receptor IL-1R8 gene eliminated the protective effects of IL-37 in the above responses. We conclude that IL-37 inhibits inflammation activation and disease severity of airway hyperreactivity by PM2.5 induction.
format	article
author	Min Wang Shujie Hou Xi Lu Jingwen Li Rongqin Li Xixin Yan
author_facet	Min Wang Shujie Hou Xi Lu Jingwen Li Rongqin Li Xixin Yan
author_sort	Min Wang
title	Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness
title_short	Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness
title_full	Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness
title_fullStr	Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness
title_full_unstemmed	Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness
title_sort	interleukin-37 inhibits inflammation activation and disease severity of pm2.5-induced airway hyperresponsiveness
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/99f1b91132d34ff8bf0bef94fe87b8d0
work_keys_str_mv	AT minwang interleukin37inhibitsinflammationactivationanddiseaseseverityofpm25inducedairwayhyperresponsiveness AT shujiehou interleukin37inhibitsinflammationactivationanddiseaseseverityofpm25inducedairwayhyperresponsiveness AT xilu interleukin37inhibitsinflammationactivationanddiseaseseverityofpm25inducedairwayhyperresponsiveness AT jingwenli interleukin37inhibitsinflammationactivationanddiseaseseverityofpm25inducedairwayhyperresponsiveness AT rongqinli interleukin37inhibitsinflammationactivationanddiseaseseverityofpm25inducedairwayhyperresponsiveness AT xixinyan interleukin37inhibitsinflammationactivationanddiseaseseverityofpm25inducedairwayhyperresponsiveness
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Interleukin-37 inhibits inflammation activation and disease severity of PM2.5-induced airway hyperresponsiveness

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