Mesenchymal stem cells ameliorate the histopathological changes in a murine model of chronic asthma


Creative Commons License

Firinci F., Karaman M., Baran Y. , Bagriyanik A., AYYILDIZ Z. A. , Kiray M., et al.

INTERNATIONAL IMMUNOPHARMACOLOGY, cilt.11, ss.1120-1126, 2011 (SCI İndekslerine Giren Dergi) identifier identifier

  • Cilt numarası: 11 Konu: 8
  • Basım Tarihi: 2011
  • Doi Numarası: 10.1016/j.intimp.2011.03.009
  • Dergi Adı: INTERNATIONAL IMMUNOPHARMACOLOGY
  • Sayfa Sayısı: ss.1120-1126

Özet

Asthma therapies are effective in reducing inflammation but airway remodeling is poorly responsive to these agents. New therapeutic options that have fewer side effects and reverse chronic changes in the lungs are essential. Mesenchymal stem cells (MSCs) are promising for the development of novel therapies in regenerative medicine. This study aimed to examine the efficacy of MSCs on lung histopathology in a murine model of chronic asthma. BALB/c mice were divided into four groups: Group 1 (control group, n = 6), Group 2 (ovalbumin induced asthma only, n = 10), Group 3 (ovalbumin induced asthma + MSCs, n = 10), and Group 4 (MSCs only, n = 10). Histological findings (basement membrane, epithelium, subepithelial smooth muscle thickness, numbers of goblet and mast cells) of the airways and MSC migration were evaluated by light, electron, and confocal microscopes. In Group 3, all early histopathological changes except epithelial thickness and all of the chronic changes were significantly ameliorated when compared with Group 2. Evaluation with confocal microscopy showed that no noteworthy amount of MSCs were present in the lung tissues of Group 4 while significant amount of MSCs was detected in Group 3. Serum NO levels in Group 3, were significantly lower than Group 2. The results of this study revealed that MSCs migrated to lung tissue and ameliorated bronchial asthma in murine model. Further studies are needed to evaluate the efficacy of MSCs for the treatment of asthma. (C) 2011 Elsevier B.V. All rights reserved.