Effects of bone marrow-derived mononuclear cells on airway and lung parenchyma remodeling in a murine model of chronic allergic inflammation

Respir Physiol Neurobiol. 2011 Jan 31;175(1):153-63. doi: 10.1016/j.resp.2010.10.006. Epub 2010 Nov 2.


We hypothesized that bone marrow-derived mononuclear cells (BMDMC) would attenuate the remodeling process in a chronic allergic inflammation model. C57BL/6 mice were assigned to two groups. In OVA, mice were sensitized and repeatedly challenged with ovalbumin. Control mice (C) received saline under the same protocol. C and OVA were further randomized to receive BMDMC (2 × 10⁶) or saline intravenously 24 h before the first challenge. BMDMC therapy reduced eosinophil infiltration, smooth muscle-specific actin expression, subepithelial fibrosis, and myocyte hypertrophy and hyperplasia, thus causing a decrease in airway hyperresponsiveness and lung mechanical parameters. BMDMC from green fluorescent protein (GFP)-transgenic mice transplanted into GFP-negative mice yielded lower engraftment in OVA. BMDMC increased insulin-like growth factor expression, but reduced interleukin-5, transforming growth factor-β, platelet-derived growth factor, and vascular endothelial growth factor mRNA expression. In conclusion, in the present chronic allergic inflammation model, BMDMC therapy was an effective pre-treatment protocol that potentiated airway epithelial cell repair and prevented inflammatory and remodeling processes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Airway Remodeling / physiology*
  • Analysis of Variance
  • Animals
  • Bone Marrow Cells / physiology*
  • Bronchoalveolar Lavage Fluid
  • Cell- and Tissue-Based Therapy / methods*
  • Chronic Disease
  • Connective Tissue / physiology*
  • Connective Tissue / ultrastructure
  • Disease Models, Animal
  • Female
  • Injections, Intravenous / methods
  • Intercellular Signaling Peptides and Proteins / metabolism
  • Interleukin-5 / metabolism
  • Leukocytes, Mononuclear / physiology*
  • Lung / pathology
  • Lung / ultrastructure
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microscopy, Electron, Transmission / methods
  • Ovalbumin / immunology
  • Respiratory Hypersensitivity / etiology
  • Respiratory Hypersensitivity / pathology
  • Respiratory Hypersensitivity / therapy*


  • Intercellular Signaling Peptides and Proteins
  • Interleukin-5
  • Ovalbumin