Modulation of nuclear factor-κB-mediated pro-inflammatory response is associated with exogenous administration of bone marrow-derived mesenchymal stem cells for treatment of experimental colitis

Mol Med Rep. 2015 Apr;11(4):2741-8. doi: 10.3892/mmr.2014.3038. Epub 2014 Dec 3.

Abstract

Mesenchymal stem cells (MSCs) inhibit the immune response in vitro and prevent the induction of disease in certain experimental models. As a result, MSC‑mediated therapy is a rapidly growing field of research. However, the efficacy of MSCs in the treatment of inflammatory bowel disease (IBD) has remained to be determined. In the present study, rats with 2,4,6‑trinitrobenzene sulfonic acid (TNBS)‑induced colitis were injected with prepared MSCs (1x106) into the tail vein. Two weeks following intravenous MSC administration, the concentration of tumor necrosis factor‑α (TNF‑α) in the serum was measured by an ELISA. The protein expression of nuclear factor‑κB (NF‑κBp65) in the colonic mucosa was assessed by western blot analysis. mRNA expression of TNF‑α and NF‑κBp65 was determined by reverse‑transcription quantitative polymerase chain reaction. MSCs were shown to exert an immunomodulatory effect on TNBS‑induced colitis and may be of use in the treatment of IBD. In addition, modulation of the NF‑κB‑mediated pro‑inflammatory response may contribute to the underlying mechanism by which MSCs ameliorate the clinical and histological changes associated with IBD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / metabolism*
  • Colitis / pathology
  • Colitis / therapy
  • Cytokines / blood
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Female
  • Gene Expression
  • Immunophenotyping
  • Inflammation Mediators / blood
  • Inflammation Mediators / metabolism*
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / metabolism*
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Phenotype
  • Rats
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • Inflammation Mediators
  • NF-kappa B
  • Tumor Necrosis Factor-alpha