Macrophage and Fibroblast Interactions in Biomaterial‐Mediated Fibrosis

Biomaterial‐mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti‐inflammatory drugs, hydrophobic co...

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Bibliographic Details
Published in:Advanced healthcare materials Vol. 8; no. 4; pp. e1801451 - n/a
Main Authors: Witherel, Claire E., Abebayehu, Daniel, Barker, Thomas H., Spiller, Kara L.
Format: Journal Article
Language:English
Published: Germany Wiley Subscription Services, Inc 01.02.2019
Subjects:
Animals
Anti-Inflammatory Agents - therapeutic use
Biocompatible Materials - adverse effects
Biocompatible Materials - pharmacology
biomaterials
Biomedical materials
Crosstalk
Drug delivery
Drug delivery systems
Encapsulation
Extracellular matrix
Extracellular Matrix - immunology
Extracellular Matrix - pathology
Fibroblasts
Fibroblasts - immunology
Fibroblasts - pathology
Fibrosis
foreign body response
Humans
Hydrophobicity
In vivo methods and tests
Inflammation
Macrophages
Macrophages - immunology
Macrophages - pathology
Regeneration
fibroblasts
macrophages
fibrosis
foreign body response
biomaterials
ISSN:2192-2640, 2192-2659, 2192-2659
Online Access:Get full text
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Abstract Biomaterial‐mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti‐inflammatory drugs, hydrophobic coatings, etc.), many materials are still subject to a foreign body response, resulting in encapsulation of dense, scar‐like extracellular matrix. The primary cells involved in biomaterial‐mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial‐mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review, the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo is investigated, with additional focus on fibroblast and macrophage crosstalk in vitro along with in vitro models to study the foreign body response. Lastly, several strategies that have been used to specifically modulate macrophage and fibroblast behavior in vitro and in vivo to control biomaterial‐mediated fibrosis are highlighted. Macrophages and fibroblasts play major roles in biomaterial‐mediated and pathological fibrosis, but their distinct phenotypes and subsequent crosstalk remain loosely defined. This review discusses the role of macrophage phenotypes in fibrosis in vivo, in vitro models to study biomaterial‐mediated fibrosis, macrophage and fibroblast crosstalk in vitro, along with biomaterial strategies to modulate macrophage and fibroblast behavior for tissue regeneration.
AbstractList Biomaterial‐mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti‐inflammatory drugs, hydrophobic coatings, etc.), many materials are still subject to a foreign body response, resulting in encapsulation of dense, scar‐like extracellular matrix. The primary cells involved in biomaterial‐mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial‐mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review, the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo is investigated, with additional focus on fibroblast and macrophage crosstalk in vitro along with in vitro models to study the foreign body response. Lastly, several strategies that have been used to specifically modulate macrophage and fibroblast behavior in vitro and in vivo to control biomaterial‐mediated fibrosis are highlighted. Macrophages and fibroblasts play major roles in biomaterial‐mediated and pathological fibrosis, but their distinct phenotypes and subsequent crosstalk remain loosely defined. This review discusses the role of macrophage phenotypes in fibrosis in vivo, in vitro models to study biomaterial‐mediated fibrosis, macrophage and fibroblast crosstalk in vitro, along with biomaterial strategies to modulate macrophage and fibroblast behavior for tissue regeneration.
Biomaterial‐mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti‐inflammatory drugs, hydrophobic coatings, etc.), many materials are still subject to a foreign body response, resulting in encapsulation of dense, scar‐like extracellular matrix. The primary cells involved in biomaterial‐mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial‐mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review, the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo is investigated, with additional focus on fibroblast and macrophage crosstalk in vitro along with in vitro models to study the foreign body response. Lastly, several strategies that have been used to specifically modulate macrophage and fibroblast behavior in vitro and in vivo to control biomaterial‐mediated fibrosis are highlighted.
Biomaterial-mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti-inflammatory drugs, hydrophobic coatings, etc.), many materials are still subject to a foreign body response, resulting in encapsulation of dense, scar-like extracellular matrix. The primary cells involved in biomaterial-mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial-mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review, the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo is investigated, with additional focus on fibroblast and macrophage crosstalk in vitro along with in vitro models to study the foreign body response. Lastly, several strategies that have been used to specifically modulate macrophage and fibroblast behavior in vitro and in vivo to control biomaterial-mediated fibrosis are highlighted.Biomaterial-mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e., delivery of anti-inflammatory drugs, hydrophobic coatings, etc.), many materials are still subject to a foreign body response, resulting in encapsulation of dense, scar-like extracellular matrix. The primary cells involved in biomaterial-mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial-mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review, the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo is investigated, with additional focus on fibroblast and macrophage crosstalk in vitro along with in vitro models to study the foreign body response. Lastly, several strategies that have been used to specifically modulate macrophage and fibroblast behavior in vitro and in vivo to control biomaterial-mediated fibrosis are highlighted.
Biomaterial-mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many biomaterial technologies that have been designed to evade or suppress inflammation (i.e. delivery of anti-inflammatory drugs, hydrophobic coatings, etc.) many materials are still subject to a foreign body response, resulting encapsulation of dense, scar-like extracellular matrix. The primary cells involved in biomaterial-mediated fibrosis are macrophages, which modulate inflammation, and fibroblasts, which primarily lay down new extracellular matrix. While macrophages and fibroblasts are implicated in driving biomaterial-mediated fibrosis, the signaling pathways and spatiotemporal crosstalk between these cell types remain loosely defined. In this review we set out to decipher the role of M1 and M2 macrophages (and soluble cues) involved in the fibrous encapsulation of biomaterials in vivo. Additionally we also focused this review on fibroblast and macrophage crosstalk in vitro, along with in vitro models to study the foreign body response. Lastly, we highlight several strategies that have been used to specifically modulate macrophages and fibroblast behavior in vitro and in vivo to control biomaterial-mediated fibrosis.
Author Barker, Thomas H.
Abebayehu, Daniel
Witherel, Claire E.
Spiller, Kara L.
Author_xml – sequence: 1
  givenname: Claire E.
  surname: Witherel
  fullname: Witherel, Claire E.
  organization: Drexel University
– sequence: 2
  givenname: Daniel
  surname: Abebayehu
  fullname: Abebayehu, Daniel
  organization: University of Virginia
– sequence: 3
  givenname: Thomas H.
  surname: Barker
  fullname: Barker, Thomas H.
  organization: University of Virginia
– sequence: 4
  givenname: Kara L.
  orcidid: 0000-0001-7798-1490
  surname: Spiller
  fullname: Spiller, Kara L.
  email: spiller@drexel.edu
  organization: Drexel University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30658015$$D View this record in MEDLINE/PubMed
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macrophages
fibrosis
foreign body response
biomaterials
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Snippet Biomaterial‐mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many...
Biomaterial-mediated inflammation and fibrosis remain a prominent challenge in designing materials to support tissue repair and regeneration. Despite the many...
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StartPage e1801451
SubjectTerms Animals
Anti-Inflammatory Agents - therapeutic use
Biocompatible Materials - adverse effects
Biocompatible Materials - pharmacology
biomaterials
Biomedical materials
Crosstalk
Drug delivery
Drug delivery systems
Encapsulation
Extracellular matrix
Extracellular Matrix - immunology
Extracellular Matrix - pathology
Fibroblasts
Fibroblasts - immunology
Fibroblasts - pathology
Fibrosis
foreign body response
Humans
Hydrophobicity
In vivo methods and tests
Inflammation
Macrophages
Macrophages - immunology
Macrophages - pathology
Regeneration
Title Macrophage and Fibroblast Interactions in Biomaterial‐Mediated Fibrosis
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fadhm.201801451
https://www.ncbi.nlm.nih.gov/pubmed/30658015
https://www.proquest.com/docview/2184123661
https://www.proquest.com/docview/2179373294
https://pubmed.ncbi.nlm.nih.gov/PMC6415913
Volume 8
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