CCL11, a novel mediator of inflammatory bone resorption

Abstract Normal bone homeostasis, which is regulated by bone-resorbing osteoclasts and bone-forming osteoblasts is perturbed by inflammation. In chronic inflammatory disease with disturbed bone remodelling, e.g. rheumatoid arthritis, patients show increased serum levels of the chemokine eotaxin-1 (C...

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Autores principales:	Elin Kindstedt, Cecilia Koskinen Holm, Rima Sulniute, Irene Martinez-Carrasco, Richard Lundmark, Pernilla Lundberg
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/73e9e9af42e74b46b995e68be52d7895
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spelling	oai:doaj.org-article:73e9e9af42e74b46b995e68be52d78952021-12-02T12:31:59ZCCL11, a novel mediator of inflammatory bone resorption10.1038/s41598-017-05654-w2045-2322https://doaj.org/article/73e9e9af42e74b46b995e68be52d78952017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05654-whttps://doaj.org/toc/2045-2322Abstract Normal bone homeostasis, which is regulated by bone-resorbing osteoclasts and bone-forming osteoblasts is perturbed by inflammation. In chronic inflammatory disease with disturbed bone remodelling, e.g. rheumatoid arthritis, patients show increased serum levels of the chemokine eotaxin-1 (CCL11). Herein, we demonstrate an inflammatory driven expression of CCL11 in bone tissue and a novel role of CCL11 in osteoclast migration and resorption. Using an inflammatory bone lesion model and primary cell cultures, we discovered that osteoblasts express CCL11 in vivo and in vitro and that expression increased during inflammatory conditions. Osteoclasts did not express CCL11, but the high affinity receptor CCR3 was significantly upregulated during osteoclast differentiation and found to colocalise with CCL11. Exogenous CCL11 was internalised in osteoclast and stimulated the migration of pre-osteoclast and concomitant increase in bone resorption. Our data pinpoints that the CCL11/CCR3 pathway could be a new target for treatment of inflammatory bone resorption.Elin KindstedtCecilia Koskinen HolmRima SulniuteIrene Martinez-CarrascoRichard LundmarkPernilla LundbergNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Elin Kindstedt Cecilia Koskinen Holm Rima Sulniute Irene Martinez-Carrasco Richard Lundmark Pernilla Lundberg CCL11, a novel mediator of inflammatory bone resorption
description	Abstract Normal bone homeostasis, which is regulated by bone-resorbing osteoclasts and bone-forming osteoblasts is perturbed by inflammation. In chronic inflammatory disease with disturbed bone remodelling, e.g. rheumatoid arthritis, patients show increased serum levels of the chemokine eotaxin-1 (CCL11). Herein, we demonstrate an inflammatory driven expression of CCL11 in bone tissue and a novel role of CCL11 in osteoclast migration and resorption. Using an inflammatory bone lesion model and primary cell cultures, we discovered that osteoblasts express CCL11 in vivo and in vitro and that expression increased during inflammatory conditions. Osteoclasts did not express CCL11, but the high affinity receptor CCR3 was significantly upregulated during osteoclast differentiation and found to colocalise with CCL11. Exogenous CCL11 was internalised in osteoclast and stimulated the migration of pre-osteoclast and concomitant increase in bone resorption. Our data pinpoints that the CCL11/CCR3 pathway could be a new target for treatment of inflammatory bone resorption.
format	article
author	Elin Kindstedt Cecilia Koskinen Holm Rima Sulniute Irene Martinez-Carrasco Richard Lundmark Pernilla Lundberg
author_facet	Elin Kindstedt Cecilia Koskinen Holm Rima Sulniute Irene Martinez-Carrasco Richard Lundmark Pernilla Lundberg
author_sort	Elin Kindstedt
title	CCL11, a novel mediator of inflammatory bone resorption
title_short	CCL11, a novel mediator of inflammatory bone resorption
title_full	CCL11, a novel mediator of inflammatory bone resorption
title_fullStr	CCL11, a novel mediator of inflammatory bone resorption
title_full_unstemmed	CCL11, a novel mediator of inflammatory bone resorption
title_sort	ccl11, a novel mediator of inflammatory bone resorption
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/73e9e9af42e74b46b995e68be52d7895
work_keys_str_mv	AT elinkindstedt ccl11anovelmediatorofinflammatoryboneresorption AT ceciliakoskinenholm ccl11anovelmediatorofinflammatoryboneresorption AT rimasulniute ccl11anovelmediatorofinflammatoryboneresorption AT irenemartinezcarrasco ccl11anovelmediatorofinflammatoryboneresorption AT richardlundmark ccl11anovelmediatorofinflammatoryboneresorption AT pernillalundberg ccl11anovelmediatorofinflammatoryboneresorption
_version_	1718394222357250048

CCL11, a novel mediator of inflammatory bone resorption

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