Journal
BIOMATERIALS
Volume 31, Issue 6, Pages 1227-1234Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2009.10.053
Keywords
Cartilage tissue engineering; Foreign body response; Immune response; Immunomodulation; Polylactic acid; Scaffold
Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [19592283]
- Establishment of Evaluation Method for Tissue Engineering
- Japan Science and Technology Agency (JST)
- New Energy and Industrial Technology Development Organization (NEDO)
- Grants-in-Aid for Scientific Research [19592283] Funding Source: KAKEN
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The immune response against biomaterials in tissue-engineered constructs could potentially worsen the outcome of tissue regeneration, but immunological reactions between host and donor in tissue-engineered constructs remain to be clarified. In the present study, we syngenically transplanted tissue-engineered cartilage constructs consisting of C57BL/6 mice auricular chondrocytes and poly-L-lactic acid scaffolds (MW:200,000) into EGFP transgenic mice of C57BL/6 background, and evaluated the response by the localization of donor-derived and host-derived cells, the latter of which were distinguished by the presence of EGFP. While donor-derived cells constituted the areas of regenerated cartilage, host-derived cells were increased in number for the initial two weeks, and then decreased and excluded to non-cartilage areas thereafter. Furthermore, EGFP positivity was mostly co-localized with that of F4/80, suggesting most of the host-derived cells in the tissue-engineered constructs could be macrophages. Immunohistochemical staining of the tissue-engineered cartilage constructs revealed expression of factors related to immune privilege in chondrocytes. such as macrophage migration inhibitory factor (MIF), fas ligand (FasL) and others. Co-culture of chondrocytes and macrophages in vitro increased the expression of MIF and FasL in the chondrocytes, suggesting that chondrocytes in tissue-engineered cartilage constructs could regulate the actions of host-derived macrophages by expressing factors related to immune privilege. (C) 2009 Elsevier Ltd. All rights reserved.
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