Culture medium from TNF-α-stimulated mesenchymal stem cells attenuates allergic conjunctivitis through multiple antiallergic mechanisms

J Allergy Clin Immunol. 2015 Aug;136(2):423-32.e8. doi: 10.1016/j.jaci.2014.12.1926. Epub 2015 Feb 1.

Abstract

Background: The immunomodulatory and anti-inflammatory functions of mesenchymal stem cells (MSCs) have been demonstrated in several autoimmune/inflammatory diseases, but their contribution to allergic conjunctivitis and underlying antiallergic mechanisms remain elusive.

Objective: We sought to explore the clinical application of MSCs to experimental allergic conjunctivitis (EAC) and its underlying antiallergic mechanisms.

Methods: Culture medium from TNF-α-stimulated, bone marrow-derived MSCs (MSC-CMT) was administered topically to mice with EAC, and the related allergic symptoms and biological changes were evaluated. Murine spleen-derived B cells, bone marrow-derived mast cells (MCs), and lung vascular endothelial cells were cultured in vitro to investigate the antiallergic MSC-CMT mechanisms.

Results: Topical instillation of MSC-CMT significantly attenuated the clinical symptoms of short ragweed pollen-induced EAC, with a significant decrease in inflammatory cell frequency, nuclear factor κB p65 expression, and TNF-α and IL-4 production. In vitro MSC-CMT significantly inhibited the activation of MCs and B-cell IgE release and reduced histamine-induced vascular hyperpermeability. During EAC, MSC-CMT treatment also decreased IgE production, histamine release, enrichment and activation of MCs, and conjunctival vascular hyperpermeability. The MSC-CMT-mediated inhibition of B cells, MCs, and histamine and its antiallergic effects during EAC were abrogated when MSCs were pretreated with COX2 small interfering RNA.

Conclusions: Our findings provide compelling evidence that MSC-CMT inhibits EAC through COX2-dependent multiple antiallergic mechanisms and support the use of MSC-CMT as a novel strategy for treating allergic conjunctivitis.

Keywords: Allergy; B cells; allergic conjunctivitis; histamine; mast cells; mesenchymal stem cells; stems cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Ambrosia / chemistry
  • Ambrosia / immunology
  • Animals
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / immunology
  • B-Lymphocytes / pathology
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / immunology
  • Bone Marrow Cells / pathology
  • Capillary Permeability / drug effects
  • Capillary Permeability / immunology
  • Cell Differentiation
  • Conjunctiva / drug effects*
  • Conjunctiva / immunology
  • Conjunctiva / pathology
  • Conjunctivitis, Allergic / chemically induced
  • Conjunctivitis, Allergic / drug therapy*
  • Conjunctivitis, Allergic / genetics
  • Conjunctivitis, Allergic / immunology
  • Culture Media, Conditioned / pharmacology*
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / immunology
  • Gene Expression Regulation
  • Histamine / metabolism
  • Immunoglobulin E / genetics
  • Interleukin-4 / genetics
  • Interleukin-4 / immunology
  • Mesenchymal Stem Cells / drug effects*
  • Mesenchymal Stem Cells / immunology
  • Mesenchymal Stem Cells / pathology
  • Mice
  • Mice, Inbred BALB C
  • Pollen / immunology
  • Primary Cell Culture
  • RNA, Small Interfering / genetics
  • RNA, Small Interfering / immunology
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Culture Media, Conditioned
  • RNA, Small Interfering
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Immunoglobulin E
  • Histamine
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2