Macrophage phenotype in response to ECM bioscaffolds

Macrophage presence and phenotype are critical determinants of the healing response following injury. Downregulation of the pro-inflammatory macrophage phenotype has been associated with the therapeutic use of bioscaffolds composed of extracellular matrix (ECM), but phenotypic characterization of m...

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Main Authors: Huleihel, Luai, Dziki, Jenna L., Bartolacci, Joseph G., Rausch, Theresa, Scarritt, Michelle E., Cramer, Madeline C., Vorobyov, Tatiana, LoPresti, Samuel T., Swinehart, Ilea T., White, Lisa J., Brown, Bryan N., Badylak, Stephen F
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Published: Elsevier 2017
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Online Access:https://eprints.nottingham.ac.uk/46384/
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author Huleihel, Luai
Dziki, Jenna L.
Bartolacci, Joseph G.
Rausch, Theresa
Scarritt, Michelle E.
Cramer, Madeline C.
Vorobyov, Tatiana
LoPresti, Samuel T.
Swinehart, Ilea T.
White, Lisa J.
Brown, Bryan N.
Badylak, Stephen F
author_facet Huleihel, Luai
Dziki, Jenna L.
Bartolacci, Joseph G.
Rausch, Theresa
Scarritt, Michelle E.
Cramer, Madeline C.
Vorobyov, Tatiana
LoPresti, Samuel T.
Swinehart, Ilea T.
White, Lisa J.
Brown, Bryan N.
Badylak, Stephen F
author_sort Huleihel, Luai
building Nottingham Research Data Repository
collection Online Access
description Macrophage presence and phenotype are critical determinants of the healing response following injury. Downregulation of the pro-inflammatory macrophage phenotype has been associated with the therapeutic use of bioscaffolds composed of extracellular matrix (ECM), but phenotypic characterization of macrophages has typically been limited to small number of non-specific cell surface markers or expressed proteins. The present study determined the response of both primary murine bone marrow derived macrophages (BMDM) and a transformed human mononuclear cell line (THP-1 cells) to degradation products of two different, commonly used ECM bioscaffolds; urinary bladder matrix (UBM-ECM) and small intestinal submucosa (SIS-ECM). Quantified cell responses included gene expression, protein expression, commonly used cell surface markers, and functional assays. Results showed that the phenotype elicited by ECM exposure (MECM) is distinct from both the classically activated IFNγ + LPS phenotype and the alternatively activated IL-4 phenotype. Furthermore, the BMDM and THP-1 macrophages responded differently to identical stimuli, and UBM-ECM and SIS-ECM bioscaffolds induced similar, yet distinct phenotypic profiles. The results of this study not only characterized an MECM phenotype that has anti-inflammatory traits but also showed the risks and challenges of making conclusions about the role of macrophage mediated events without consideration of the source of macrophages and the limitations of individual cell markers.
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spelling nottingham-463842020-05-04T19:58:42Z https://eprints.nottingham.ac.uk/46384/ Macrophage phenotype in response to ECM bioscaffolds Huleihel, Luai Dziki, Jenna L. Bartolacci, Joseph G. Rausch, Theresa Scarritt, Michelle E. Cramer, Madeline C. Vorobyov, Tatiana LoPresti, Samuel T. Swinehart, Ilea T. White, Lisa J. Brown, Bryan N. Badylak, Stephen F Macrophage presence and phenotype are critical determinants of the healing response following injury. Downregulation of the pro-inflammatory macrophage phenotype has been associated with the therapeutic use of bioscaffolds composed of extracellular matrix (ECM), but phenotypic characterization of macrophages has typically been limited to small number of non-specific cell surface markers or expressed proteins. The present study determined the response of both primary murine bone marrow derived macrophages (BMDM) and a transformed human mononuclear cell line (THP-1 cells) to degradation products of two different, commonly used ECM bioscaffolds; urinary bladder matrix (UBM-ECM) and small intestinal submucosa (SIS-ECM). Quantified cell responses included gene expression, protein expression, commonly used cell surface markers, and functional assays. Results showed that the phenotype elicited by ECM exposure (MECM) is distinct from both the classically activated IFNγ + LPS phenotype and the alternatively activated IL-4 phenotype. Furthermore, the BMDM and THP-1 macrophages responded differently to identical stimuli, and UBM-ECM and SIS-ECM bioscaffolds induced similar, yet distinct phenotypic profiles. The results of this study not only characterized an MECM phenotype that has anti-inflammatory traits but also showed the risks and challenges of making conclusions about the role of macrophage mediated events without consideration of the source of macrophages and the limitations of individual cell markers. Elsevier 2017-02 Article PeerReviewed Huleihel, Luai, Dziki, Jenna L., Bartolacci, Joseph G., Rausch, Theresa, Scarritt, Michelle E., Cramer, Madeline C., Vorobyov, Tatiana, LoPresti, Samuel T., Swinehart, Ilea T., White, Lisa J., Brown, Bryan N. and Badylak, Stephen F (2017) Macrophage phenotype in response to ECM bioscaffolds. Seminars in Immunology, 29 . pp. 2-13. ISSN 1096-3618 ECM (extracellular matrix); macrophages; activation; THP-1; BMDM; phenotype http://www.sciencedirect.com/science/article/pii/S1044532316301129?via%3Dihub doi:10.1016/j.smim.2017.04.004 doi:10.1016/j.smim.2017.04.004
spellingShingle ECM (extracellular matrix); macrophages; activation; THP-1; BMDM; phenotype
Huleihel, Luai
Dziki, Jenna L.
Bartolacci, Joseph G.
Rausch, Theresa
Scarritt, Michelle E.
Cramer, Madeline C.
Vorobyov, Tatiana
LoPresti, Samuel T.
Swinehart, Ilea T.
White, Lisa J.
Brown, Bryan N.
Badylak, Stephen F
Macrophage phenotype in response to ECM bioscaffolds
title Macrophage phenotype in response to ECM bioscaffolds
title_full Macrophage phenotype in response to ECM bioscaffolds
title_fullStr Macrophage phenotype in response to ECM bioscaffolds
title_full_unstemmed Macrophage phenotype in response to ECM bioscaffolds
title_short Macrophage phenotype in response to ECM bioscaffolds
title_sort macrophage phenotype in response to ecm bioscaffolds
topic ECM (extracellular matrix); macrophages; activation; THP-1; BMDM; phenotype
url https://eprints.nottingham.ac.uk/46384/
https://eprints.nottingham.ac.uk/46384/
https://eprints.nottingham.ac.uk/46384/