Biomimetic collagenous scaffold to tune inflammation by targeting macrophages

The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Francesca Taraballi [verfasserIn] Bruna Corradetti [verfasserIn] Silvia Minardi [verfasserIn] Sebastian Powel [verfasserIn] Fernando Cabrera [verfasserIn] Jeff L. Van Eps [verfasserIn] Bradley K Weiner [verfasserIn] Ennio Tasciotti [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Übergeordnetes Werk:	In: Journal of Tissue Engineering - SAGE Publishing, 2010, 7(2016)
Übergeordnetes Werk:	volume:7 ; year:2016

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1177/2041731415624667

Katalog-ID:	DOAJ053154533

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allfields	10.1177/2041731415624667 doi (DE-627)DOAJ053154533 (DE-599)DOAJ217cd3abc2fd4b00ab96f6d6bea4eb43 DE-627 ger DE-627 rakwb eng QD415-436 Francesca Taraballi verfasserin aut Biomimetic collagenous scaffold to tune inflammation by targeting macrophages 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair. Biochemistry Bruna Corradetti verfasserin aut Silvia Minardi verfasserin aut Sebastian Powel verfasserin aut Fernando Cabrera verfasserin aut Jeff L. Van Eps verfasserin aut Bradley K Weiner verfasserin aut Ennio Tasciotti verfasserin aut In Journal of Tissue Engineering SAGE Publishing, 2010 7(2016) (DE-627)635606240 (DE-600)2573915-3 20417314 nnns volume:7 year:2016 https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/article/217cd3abc2fd4b00ab96f6d6bea4eb43 kostenfrei https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/toc/2041-7314 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016
spelling	10.1177/2041731415624667 doi (DE-627)DOAJ053154533 (DE-599)DOAJ217cd3abc2fd4b00ab96f6d6bea4eb43 DE-627 ger DE-627 rakwb eng QD415-436 Francesca Taraballi verfasserin aut Biomimetic collagenous scaffold to tune inflammation by targeting macrophages 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair. Biochemistry Bruna Corradetti verfasserin aut Silvia Minardi verfasserin aut Sebastian Powel verfasserin aut Fernando Cabrera verfasserin aut Jeff L. Van Eps verfasserin aut Bradley K Weiner verfasserin aut Ennio Tasciotti verfasserin aut In Journal of Tissue Engineering SAGE Publishing, 2010 7(2016) (DE-627)635606240 (DE-600)2573915-3 20417314 nnns volume:7 year:2016 https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/article/217cd3abc2fd4b00ab96f6d6bea4eb43 kostenfrei https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/toc/2041-7314 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016
allfields_unstemmed	10.1177/2041731415624667 doi (DE-627)DOAJ053154533 (DE-599)DOAJ217cd3abc2fd4b00ab96f6d6bea4eb43 DE-627 ger DE-627 rakwb eng QD415-436 Francesca Taraballi verfasserin aut Biomimetic collagenous scaffold to tune inflammation by targeting macrophages 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair. Biochemistry Bruna Corradetti verfasserin aut Silvia Minardi verfasserin aut Sebastian Powel verfasserin aut Fernando Cabrera verfasserin aut Jeff L. Van Eps verfasserin aut Bradley K Weiner verfasserin aut Ennio Tasciotti verfasserin aut In Journal of Tissue Engineering SAGE Publishing, 2010 7(2016) (DE-627)635606240 (DE-600)2573915-3 20417314 nnns volume:7 year:2016 https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/article/217cd3abc2fd4b00ab96f6d6bea4eb43 kostenfrei https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/toc/2041-7314 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016
allfieldsGer	10.1177/2041731415624667 doi (DE-627)DOAJ053154533 (DE-599)DOAJ217cd3abc2fd4b00ab96f6d6bea4eb43 DE-627 ger DE-627 rakwb eng QD415-436 Francesca Taraballi verfasserin aut Biomimetic collagenous scaffold to tune inflammation by targeting macrophages 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair. Biochemistry Bruna Corradetti verfasserin aut Silvia Minardi verfasserin aut Sebastian Powel verfasserin aut Fernando Cabrera verfasserin aut Jeff L. Van Eps verfasserin aut Bradley K Weiner verfasserin aut Ennio Tasciotti verfasserin aut In Journal of Tissue Engineering SAGE Publishing, 2010 7(2016) (DE-627)635606240 (DE-600)2573915-3 20417314 nnns volume:7 year:2016 https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/article/217cd3abc2fd4b00ab96f6d6bea4eb43 kostenfrei https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/toc/2041-7314 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016
allfieldsSound	10.1177/2041731415624667 doi (DE-627)DOAJ053154533 (DE-599)DOAJ217cd3abc2fd4b00ab96f6d6bea4eb43 DE-627 ger DE-627 rakwb eng QD415-436 Francesca Taraballi verfasserin aut Biomimetic collagenous scaffold to tune inflammation by targeting macrophages 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair. Biochemistry Bruna Corradetti verfasserin aut Silvia Minardi verfasserin aut Sebastian Powel verfasserin aut Fernando Cabrera verfasserin aut Jeff L. Van Eps verfasserin aut Bradley K Weiner verfasserin aut Ennio Tasciotti verfasserin aut In Journal of Tissue Engineering SAGE Publishing, 2010 7(2016) (DE-627)635606240 (DE-600)2573915-3 20417314 nnns volume:7 year:2016 https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/article/217cd3abc2fd4b00ab96f6d6bea4eb43 kostenfrei https://doi.org/10.1177/2041731415624667 kostenfrei https://doaj.org/toc/2041-7314 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2889 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016
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callnumber-first	Q - Science
author	Francesca Taraballi
spellingShingle	Francesca Taraballi misc QD415-436 misc Biochemistry Biomimetic collagenous scaffold to tune inflammation by targeting macrophages
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topic_title	QD415-436 Biomimetic collagenous scaffold to tune inflammation by targeting macrophages
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title	Biomimetic collagenous scaffold to tune inflammation by targeting macrophages
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title_full	Biomimetic collagenous scaffold to tune inflammation by targeting macrophages
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title_sort	biomimetic collagenous scaffold to tune inflammation by targeting macrophages
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title_auth	Biomimetic collagenous scaffold to tune inflammation by targeting macrophages
abstract	The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair.
abstractGer	The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair.
abstract_unstemmed	The inflammatory response following implantation of a biomaterial is one of the major regulatory aspects of the overall regenerative process. The progress of inflammation determines whether functional tissue is restored or if nonfunctional fibrotic tissue is formed. This delicate balance is directed by the activity of different cells. Among these, macrophages and their different phenotypes, the inflammatory M1 to anti-inflammatory M2, are considered key players in the process. Recent approaches exploit macrophage’s regenerative potential in tissue engineering. Here, we propose a collagen scaffold functionalized with chondroitin sulfate (CSCL), a glycosaminoglycan known to be able to tune inflammation. We studied CSCL effects on bone-marrow-derived macrophages in physiological, and lipopolysaccharides-inflamed, conditions in vitro. Our data demonstrate that CSCL is able to modulate macrophage phenotype by inhibiting the LPS/CD44/NF-kB cascade. As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. The present work provides indications regarding the immunomodulatory potential of molecules used for the development of biomimetic materials and suggests their use to direct macrophage immune modulation for tissue repair.
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title_short	Biomimetic collagenous scaffold to tune inflammation by targeting macrophages
url	https://doi.org/10.1177/2041731415624667 https://doaj.org/article/217cd3abc2fd4b00ab96f6d6bea4eb43 https://doaj.org/toc/2041-7314
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As a consequence, an upregulation of anti-inflammatory markers ( TGF-β , Arg , MRC1 , and IL-10 ) was found concomitantly with a decrease in the expression of pro-inflammatory markers ( iNOS , TNF-α , IL-1β , IL-12β ). We then implanted CSCL subcutaneously in a rat model to test whether the same molecular mechanism could be maintained in an in vivo environment. In vivo data confirmed the in vitro studies. A significant reduction in the number of infiltrating cells around and within the implants was observed at 72 h, with a significant downregulation of pro-inflammatory genes expression. 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