Prednisolone decreases cellular adhesion molecules required for inflammatory cell infiltration in dystrophin-deficient skeletal muscle

Michelle Wehling-Henricks, James J. Lee, James G. Tidball

Research output: Contribution to journalArticle

58 Scopus citations

Abstract

The mechanism of prednisolone's efficacy in the dystrophic pathology is unclear. Prednisolone's anti-inflammatory functions may be particularly important considering the significance of inflammatory cells in dystrophinopathy. In other pathologies, prednisolone's anti-inflammatory effects can be mediated by reducing cellular adhesion molecule (CAM) expression. The goal of this study was to examine the effects of prednisolone on inflammation and CAM expression in dystrophic muscle. Dystrophin-deficient, mdx mice were treated with 0.75 mg/kg prednisolone from 2 to 4 weeks of age. Prednisolone reduced macrophages (-59%, -57%), CD4 + T-cells (-50%, -60%), CD8 + T-cells (-58%, -48%), and eosinophils (-36%, -25%) in quadriceps and soleus muscles, respectively. Prednisolone-treated mice also exhibited decreased vascular P-selectin (-82%) and ICAM-1 (-52%) expression and fewer L-selectin (-79%) and ICAM-1 (-57%) expressing mononuclear cells in quadriceps. Prednisolone reduced sarcolemmal damage and degeneration as well. Our data show that prednisolone is an effective anti-inflammatory in dystrophic muscle and may function by modulating CAM expression.

Original languageEnglish (US)
Pages (from-to)483-490
Number of pages8
JournalNeuromuscular Disorders
Volume14
Issue number8-9
DOIs
StatePublished - Sep 1 2004

Keywords

  • Inflammation
  • Mouse
  • Muscular dystrophy
  • Prednisolone
  • mdx

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Neurology
  • Clinical Neurology
  • Genetics(clinical)

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