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Cited by 273Mast cells and histamineTissue Engineering and Regenerative MedicineOrthopaedic implants and arthroplasty

Mast cells mediate acute inflammatory responses to implanted biomaterials

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Tang, Liping, Jennings, Timothy A., Eaton, John W.·1998·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.95.15.8841PMC PMC21164
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Abstract

Implanted biomaterials trigger acute and chronic inflammatory responses. The mechanisms involved in such acute inflammatory responses can be arbitrarily divided into phagocyte transmigration, chemotaxis, and adhesion to implant surfaces. We earlier observed that two chemokines-macrophage inflammatory protein 1alpha/monocyte chemoattractant protein 1-and the phagocyte integrin Mac-1 (CD11b/CD18)/surface fibrinogen interaction are, respectively, required for phagocyte chemotaxis and adherence to biomaterial surfaces. However, it is still not clear how the initial transmigration of phagocytes through the endothelial barrier into the area of the implant is triggered. Because implanted biomaterials elicit histaminic responses in the surrounding tissue, and histamine release is known to promote rapid diapedesis of inflammatory cells, we evaluated the possible role of histamine and mast cells in the recruitment of phagocytes to biomaterial implants. Using i.p. and s. c. implantation of polyethylene terephthalate disks in mice we find: (i) Extensive degranulation of mast cells, accompanied by histamine release, occurs adjacent to short-term i.p. implants. (ii) Simultaneous administration of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respectively) greatly diminishes recruitment and adhesion of both neutrophils (<20% of control) and monocytes/macrophages (<30% of control) to implants. (iii) Congenitally mast cell-deficient mice also exhibit markedly reduced accumulation of phagocytes on both i.p. and s.c implants. (iv) Finally, mast cell reconstitution of mast cell-deficient mice restores "normal" inflammatory responses to biomaterial implants. We conclude that mast cells and their granular products, especially histamine, are important in recruitment of inflammatory cells to biomaterial implants. Improved knowledge of such responses may permit purposeful modulation of both acute and chronic inflammation affecting implanted biomaterials.

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  • Recruitment of inflammatory cells is mediated by mast cells, which secrete granular products that attract and promote adhesion of monocytes and macrophages to the implant.

    “The recruitment is mediated by mast cells, which secrete granular products that attract and promote the adhesion of monocytes and macrophages to the implant.[ 34 ]”

    From Unraveling and Harnessing the Immune Response at the Cell–Biomaterial Interface for Tissue Engineering Purposes (2024) · cites this paper as [34]

    The Abstract reports that mast cells and their granular products, especially histamine, are important in recruiting inflammatory cells to implants. The Discussion distinguishes that role from chemotaxis toward the implant, which it attributes to chemokines, and adhesion to the implant surface, which it attributes at least partly to phagocyte Mac-1 binding surface fibrinogen. Thus, the source does not support assigning attraction and implant-surface adhesion to mast-cell granular products. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Mast cell degranulation with histamine release and fibrinogen adsorption mediates acute inflammatory responses to implanted biomaterials.

    “Mast cell degranulation with histamine release and fibrinogen adsorption is known to mediate acute inflammatory responses to implanted biomaterials.[6, 7]”

    From Foreign body reaction to biomaterials (2008) · cites this paper as [7]

  • Mast cell degranulation and release of histamine plays an integral role in recruiting phagocytes, including macrophages, to the site of the implanted biomaterial.

    “In addition, mast cell degranulation and release of histamine has been shown to play an integral role in recruiting phagocytes, including macrophages, to the site of the implanted biomaterial.[7]”

    From Foreign body reaction to biomaterials (2008) · cites this paper as [7]

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Authors
Tang, L., Jennings, T. A., & Eaton, J. W.
Affiliations
Baylor College of Medicine (US)
ORCID
Tang, Liping
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1998-07-21
Volume
95
Issue
15
Pages
8841-8846
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.95.15.8841
PMC
PMC21164
OpenAlex
W2037046845
Cited by
272
References
78
Citations by year
2026: 1 · 2025: 8 · 2024: 8 · 2023: 6 · 2022: 4 · 2021: 18 · 2020: 19 · 2019: 8 · 2018: 11 · 2017: 19 · 2016: 16 · 2015: 12 · 2014: 8 · 2013: 14 · 2012: 8
FWCI
1.56
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
  • Health Sciences › Medicine › Surgery › Tissue Engineering and Regenerative Medicine
  • Health Sciences › Medicine › Surgery › Orthopaedic implants and arthroplasty
Keywords
mast cells, histamine, biomaterial implantation, acute inflammation, phagocyte recruitment, neutrophil transmigration, monocyte adhesion, histamine H1 receptor antagonists, H2 receptor antagonists, mast cell-deficient mice, transendothelial migration, macrophage inflammatory protein-1alpha, Mac-1
MeSH terms
Animals, Biocompatible Materials, Histamine, Histamine Release, Inflammation, Mast Cells, Phagocytes, Cell Degranulation, Mice

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