Exploring the time-dependent changes to skeletal muscle macrophage redox homeostasis in Myositis

Myositis, a rare idiopathic inflammatory myopathy (IIM), is characterized by skeletal muscle wasting and weakness. While autoimmune-mediated, the etiology is largely unknown. The focus of this thesis was to assess a modified version of a model commonly used in the literature, known as experimental autoimmune myositis. We assessed the progression of this model over time in the gastrocnemius and soleus muscles, to explore muscle specific changes in the immune response. Our findings reveal changes to ROS production in muscle macrophages, as well alterations in the expression of inflammatory related genes. However, the modified model, with the absence of pertussis toxin, does not replicate the strong disease phenotype observed in traditional EAM models. This allows us to question the extent to which pertussis toxin induces a myositis phenotype as opposed to systemic inflammation. Ultimately, there is a need to develop a comprehensive model of myositis that accurately mimics the human condition.