Research Article A Mathematical Model of Skeletal Muscle Disease and Immune Response in the mdx Mouse Abdul Salam Jarrah, 1 Filippo Castiglione, 2 Nicholas P. Evans, 3 Robert W. Grange, 4 and Reinhard Laubenbacher 5,6 1 Department of Mathematics and Statistics, American University of Sharjah, Sharjah 26666, UAE 2 Institute for Applied Mathematics, National Research Council of Italy, 00185 Rome, Italy 3 Department of Population Health Sciences, Virginia Tech, Blacksburg, VA 24060, USA 4 Department of Human Nutrition, Foods and Exercise, Virginia Tech, Blacksburg, VA 24060, USA 5 Center of Quantitative Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA 6 Jackson Laboratory for Genomic Medicine, Farmington, CT 06030, USA Correspondence should be addressed to Abdul Salam Jarrah; ajarrah@aus.edu Received 30 March 2014; Accepted 19 May 2014; Published 11 June 2014 Academic Editor: Francesco Pappalardo Copyright © 2014 Abdul Salam Jarrah et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Duchenne muscular dystrophy (DMD) is a genetic disease that results in the death of afected boys by early adulthood. he genetic defect responsible for DMD has been known for over 25 years, yet at present there is neither cure nor efective treatment for DMD. During early disease onset, the mdx mouse has been validated as an animal model for DMD and use of this model has led to valuable but incomplete insights into the disease process. For example, immune cells are thought to be responsible for a signiicant portion of muscle cell death in the mdx mouse; however, the role and time course of the immune response in the dystrophic process have not been well described. In this paper we constructed a simple mathematical model to investigate the role of the immune response in muscle degeneration and subsequent regeneration in the mdx mouse model of Duchenne muscular dystrophy. Our model suggests that the immune response contributes substantially to the muscle degeneration and regeneration processes. Furthermore, the analysis of the model predicts that the immune system response oscillates throughout the life of the mice, and the damaged ibers are never completely cleared. 1. Background Duchenne muscular dystrophy (DMD) is a lethal, X- chromosome muscle wasting disease afecting approximately one in 3,500 boys [1, 2]. Patients appear clinically normal at birth with the exception of elevated serum creatine kinase levels. he onset of DMD begins in early childhood with the irst observed symptoms between two and ive years of age. Typically by the age of 12, DMD patients require the use of a wheelchair due to the loss of lower limb muscle strength. Progressive weakness of the arms and legs, along with kyphoscoliosis, continues through late disease progression. Many patients die in their late teens or early twenties due to respiratory or cardiac complications [1, 3]. Currently, there are no efective means of therapy or treatment for DMD. In 1984, Bulield et al. identiied a spontaneous mutation in C57BL/10ScSn inbred mice that exhibited a disease state similar to human DMD [4]. he X chromosome-linked mutation resulted in mice (mdx mice) with high serum levels of muscle enzymes and with histological lesions comparable to those seen in human muscular dystrophy. his mutation in the murine dystrophin gene caused an absence of dystrophin in skeletal muscle and this key defect validated the mdx mouse as a suitable model of the early onset of DMD human disease [5, 6]. he histology and time course of the disease in mdx mouse model are very diferent from those in DMD patients: relatively normal life span and overall itness compared to progressive physical impairment leading to death in DMD patients [7]. Nonetheless, the mdx mouse model is regarded Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 871810, 11 pages http://dx.doi.org/10.1155/2014/871810