Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity

Abstract Microbiota maintains host tissue homeostasis and influences tissue-resident macrophages. However, the mechanisms by which commensal bacteria in regulating the alveolar macrophages remain unclear. Here, by using an antibiotic-treated (Abt) mouse model, we found commensal bacteria depletion i...

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Autores principales:	Min Cheng, Yongyan Chen, Liang Wang, Wen Chen, Ling Yang, Guodong Shen, Tingjuan Xu, Gan Shen, Zhigang Tian, Shilian Hu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9c8a76789893488ba9413d6b6064ebc6
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spelling	oai:doaj.org-article:9c8a76789893488ba9413d6b6064ebc62021-12-02T12:32:15ZCommensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity10.1038/s41598-017-08264-82045-2322https://doaj.org/article/9c8a76789893488ba9413d6b6064ebc62017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08264-8https://doaj.org/toc/2045-2322Abstract Microbiota maintains host tissue homeostasis and influences tissue-resident macrophages. However, the mechanisms by which commensal bacteria in regulating the alveolar macrophages remain unclear. Here, by using an antibiotic-treated (Abt) mouse model, we found commensal bacteria depletion induced lower frequencies and numbers of alveolar macrophages. This effect was accompanied by the altered levels of genes involved in several biological pathways, including M2 macrophage polarization, as determined by gene expression analysis. Alveolar macrophages from the Abt mice had higher protein and gene levels of Arg1, CCL24, IL-13, IL-10, IL-6 and IL-1β, which could be recovered to normal levels by reconstructing commensal bacteria in the upper respiratory of Abt mice. Moreover, alveolar macrophages performed significant enhancement of M2 functions, especially CCL24 secretion, in the Abt mice challenged with B16/F10 melanoma. Adoptive transfer of normal alveolar macrophages or antibody neutralization of CCL24 significantly recovered the decrease of γδT17 cells and rescued the defect anti-tumor response of Abt mice, indicating the elevated amount of alveolar macrophage-derived CCL24 inhibited γδT cell mediated anti-tumor response. In conclusion, we demonstrated the ability of commensal bacteria to maintain alveolar macrophages with a low level of CCL24 production, which was necessary for the normal anti-tumor response in the lung.Min ChengYongyan ChenLiang WangWen ChenLing YangGuodong ShenTingjuan XuGan ShenZhigang TianShilian HuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Min Cheng Yongyan Chen Liang Wang Wen Chen Ling Yang Guodong Shen Tingjuan Xu Gan Shen Zhigang Tian Shilian Hu Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity
description	Abstract Microbiota maintains host tissue homeostasis and influences tissue-resident macrophages. However, the mechanisms by which commensal bacteria in regulating the alveolar macrophages remain unclear. Here, by using an antibiotic-treated (Abt) mouse model, we found commensal bacteria depletion induced lower frequencies and numbers of alveolar macrophages. This effect was accompanied by the altered levels of genes involved in several biological pathways, including M2 macrophage polarization, as determined by gene expression analysis. Alveolar macrophages from the Abt mice had higher protein and gene levels of Arg1, CCL24, IL-13, IL-10, IL-6 and IL-1β, which could be recovered to normal levels by reconstructing commensal bacteria in the upper respiratory of Abt mice. Moreover, alveolar macrophages performed significant enhancement of M2 functions, especially CCL24 secretion, in the Abt mice challenged with B16/F10 melanoma. Adoptive transfer of normal alveolar macrophages or antibody neutralization of CCL24 significantly recovered the decrease of γδT17 cells and rescued the defect anti-tumor response of Abt mice, indicating the elevated amount of alveolar macrophage-derived CCL24 inhibited γδT cell mediated anti-tumor response. In conclusion, we demonstrated the ability of commensal bacteria to maintain alveolar macrophages with a low level of CCL24 production, which was necessary for the normal anti-tumor response in the lung.
format	article
author	Min Cheng Yongyan Chen Liang Wang Wen Chen Ling Yang Guodong Shen Tingjuan Xu Gan Shen Zhigang Tian Shilian Hu
author_facet	Min Cheng Yongyan Chen Liang Wang Wen Chen Ling Yang Guodong Shen Tingjuan Xu Gan Shen Zhigang Tian Shilian Hu
author_sort	Min Cheng
title	Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity
title_short	Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity
title_full	Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity
title_fullStr	Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity
title_full_unstemmed	Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity
title_sort	commensal microbiota maintains alveolar macrophages with a low level of ccl24 production to generate anti-metastatic tumor activity
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/9c8a76789893488ba9413d6b6064ebc6
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Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity

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