Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices

Abstract Neutrophil trafficking in tissues critically regulates the body’s immune response. Neutrophil migration can either play a protective role in host defense or cause health problems. Fibroblast growth factor 23 (FGF23) is a known biomarker for chronic kidney disease (CKD) and was recently show...

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Autores principales:	Ke Yang, Hagit Peretz-Soroka, Jiandong Wu, Ling Zhu, Xueling Cui, Michael Zhang, Claudio Rigatto, Yong Liu, Francis Lin
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/588fc93de11a45d0b6b7aed1cf51a249
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spelling	oai:doaj.org-article:588fc93de11a45d0b6b7aed1cf51a2492021-12-02T12:30:26ZFibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices10.1038/s41598-017-03210-02045-2322https://doaj.org/article/588fc93de11a45d0b6b7aed1cf51a2492017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03210-0https://doaj.org/toc/2045-2322Abstract Neutrophil trafficking in tissues critically regulates the body’s immune response. Neutrophil migration can either play a protective role in host defense or cause health problems. Fibroblast growth factor 23 (FGF23) is a known biomarker for chronic kidney disease (CKD) and was recently shown to impair neutrophil arrest on endothelium and transendothelial migration. In the present study, we further examined the effect of FGF23 on human blood neutrophil chemotaxis using two new microfluidic devices. Our results showed that chemotaxis of FGF23 pre-treated neutrophils to a fMLP gradient, in the presence or absence of a uniform FGF23 background, is quantitatively lower compared to the control cells. This effect is accompanied with a stronger drifting of FGF23 pre-treated cells along the flow. However, without the FGF23 pre-treatment, the FGF23 background only reduces chemotaxis of transmigrated cells through the thin barrier channel to the fMLP gradient. The effect of FGF23 on neutrophil migration and the correlation between multiple cell migration parameters are further revealed by chemotactic entropy and principle component analysis. Collectively, these results revealed the effect of FGF23 on weakening neutrophil chemotaxis, which shed light on FGF23 mediated neutrophil migration with direct disease relevance such as CKD.Ke YangHagit Peretz-SorokaJiandong WuLing ZhuXueling CuiMichael ZhangClaudio RigattoYong LiuFrancis LinNature 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 Ke Yang Hagit Peretz-Soroka Jiandong Wu Ling Zhu Xueling Cui Michael Zhang Claudio Rigatto Yong Liu Francis Lin Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
description	Abstract Neutrophil trafficking in tissues critically regulates the body’s immune response. Neutrophil migration can either play a protective role in host defense or cause health problems. Fibroblast growth factor 23 (FGF23) is a known biomarker for chronic kidney disease (CKD) and was recently shown to impair neutrophil arrest on endothelium and transendothelial migration. In the present study, we further examined the effect of FGF23 on human blood neutrophil chemotaxis using two new microfluidic devices. Our results showed that chemotaxis of FGF23 pre-treated neutrophils to a fMLP gradient, in the presence or absence of a uniform FGF23 background, is quantitatively lower compared to the control cells. This effect is accompanied with a stronger drifting of FGF23 pre-treated cells along the flow. However, without the FGF23 pre-treatment, the FGF23 background only reduces chemotaxis of transmigrated cells through the thin barrier channel to the fMLP gradient. The effect of FGF23 on neutrophil migration and the correlation between multiple cell migration parameters are further revealed by chemotactic entropy and principle component analysis. Collectively, these results revealed the effect of FGF23 on weakening neutrophil chemotaxis, which shed light on FGF23 mediated neutrophil migration with direct disease relevance such as CKD.
format	article
author	Ke Yang Hagit Peretz-Soroka Jiandong Wu Ling Zhu Xueling Cui Michael Zhang Claudio Rigatto Yong Liu Francis Lin
author_facet	Ke Yang Hagit Peretz-Soroka Jiandong Wu Ling Zhu Xueling Cui Michael Zhang Claudio Rigatto Yong Liu Francis Lin
author_sort	Ke Yang
title	Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
title_short	Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
title_full	Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
title_fullStr	Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
title_full_unstemmed	Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
title_sort	fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/588fc93de11a45d0b6b7aed1cf51a249
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_version_	1718394399277187072

Fibroblast growth factor 23 weakens chemotaxis of human blood neutrophils in microfluidic devices

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