Exploring the role of mitochondria and muscle function in a pertussis toxin free experimental autoimmune myositis mouse model

Myositis is a rare autoimmune disorder characterized by skeletal muscle inflammation and weakness. Recently, mitochondrial stress has emerged as a possible disease contributor. To assess the relationship between mitochondrial stress and myopathy in myositis, evaluations of experimental models are required. Several models utilize an exotoxin, pertussis toxin(PT), coupled with foreign myosin injections. However, PT induces systemic inflammation impacting the ability to determine if the inflammatory response is consistent with myositis or a systemic response. Thus, the purpose of this thesis is to establish a modified myositis model whereby PT is excluded to exemplify the human condition, and to explore mitochondrial stress and myopathy. This modified model demonstrated no muscle atrophy occurred, but both the diaphragm and tibialis anterior(TA) displayed indices of mitochondrial stress. Additionally, the TA exhibited weakness that recovered over time. Suggesting the modified myositis model may induce a mild phenotype, highlighting the need for more robust model development.