Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.

Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristic...

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Autores principales:	Fengjiao Yuan, Xiao Fu, Hengfei Shi, Guopu Chen, Ping Dong, Weiyun Zhang
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/25af7d2971c44df9a4142b58e120399d
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spelling	oai:doaj.org-article:25af7d2971c44df9a4142b58e120399d2021-11-25T06:01:28ZInduction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.1932-620310.1371/journal.pone.0107063https://doaj.org/article/25af7d2971c44df9a4142b58e120399d2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25198511/?tool=EBIhttps://doaj.org/toc/1932-6203Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.Fengjiao YuanXiao FuHengfei ShiGuopu ChenPing DongWeiyun ZhangPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 9, p e107063 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Fengjiao Yuan Xiao Fu Hengfei Shi Guopu Chen Ping Dong Weiyun Zhang Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
description	Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS) or cigarette smoke extract (CSE). The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS) and nitric oxide (NO) and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.
format	article
author	Fengjiao Yuan Xiao Fu Hengfei Shi Guopu Chen Ping Dong Weiyun Zhang
author_facet	Fengjiao Yuan Xiao Fu Hengfei Shi Guopu Chen Ping Dong Weiyun Zhang
author_sort	Fengjiao Yuan
title	Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
title_short	Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
title_full	Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
title_fullStr	Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
title_full_unstemmed	Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.
title_sort	induction of murine macrophage m2 polarization by cigarette smoke extract via the jak2/stat3 pathway.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/25af7d2971c44df9a4142b58e120399d
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Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.

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