Human Bone Marrow Mesenchymal Stem/Stromal Cells Exposed to an Inflammatory Environment Increase the Expression of ICAM-1 and Release Microvesicles Enriched in This Adhesive Molecule: Analysis of the Participation of TNF- α and IFN- γ

J Immunol Res. 2020 Nov 30:2020:8839625. doi: 10.1155/2020/8839625. eCollection 2020.

Abstract

Bone marrow mesenchymal stem/stromal cells (BM-MSCs) have immunoregulatory capacity; therefore, they have been used in different clinical protocols in which it is necessary to decrease the immune response. This capacity is mainly regulated by TNF-α and IFN-γ, and it has been observed that cell-cell contact, mainly mediated by ICAM-1, is important for MSCs to carry out efficient immunoregulation. Therefore, in the present work, we analyzed the effect of TNF-α alone or in combination with IFN-γ on the expression of ICAM-1. Besides, given the importance of cell contact in the immunoregulatory function of MSCs, we analyzed whether these cells release ICAM-1+ microvesicles (MVs). Our results show for the first time that TNF-α is capable of increasing the early expression of ICAM-1 in human BM-MSCs. Also, we observed that TNF-α and IFN-γ have a synergistic effect on the increase in the expression of ICAM-1. Furthermore, we found that BM-MSCs exposed to an inflammatory environment release MVs enriched in ICAM-1 (MVs-ICAM-1high). The knowledge generated in this study will contribute to the improvement of in vitro conditioning protocols that favor the therapeutic effect of these cells or their products.

MeSH terms

  • Biomarkers
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / metabolism
  • Cell-Derived Microparticles / metabolism*
  • Cellular Microenvironment*
  • Cytokines / metabolism
  • Disease Susceptibility
  • Histocompatibility Antigens Class I / genetics
  • Histocompatibility Antigens Class I / immunology
  • Humans
  • Immunophenotyping
  • Inflammation / etiology
  • Inflammation / metabolism*
  • Inflammation / pathology
  • Inflammation Mediators / metabolism
  • Intercellular Adhesion Molecule-1 / genetics*
  • Interferon-gamma / metabolism
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / metabolism
  • Mesenchymal Stem Cells / metabolism*
  • Models, Biological
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Biomarkers
  • Cell Adhesion Molecules
  • Cytokines
  • Histocompatibility Antigens Class I
  • ICAM1 protein, human
  • Inflammation Mediators
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Interferon-gamma