Deficient skeletal muscle regeneration after injury induced by a Clostridium perfringens strain associated with gas gangrene
Very little is known about the muscle regeneration process that follows myonecrosis induced by C. perfringens, the main agent of gas gangrene. This study revealed that, in a murine model of the infection with a sublethal inoculum of C. perfringens, muscle necrosis occurs concomitantly with significant vascular damage, which limits the migration of inflammatory cells. A significant increase in cytokines that promote inflammation explains the presence of inflammatory infiltrate; however, an impaired IFN{gamma} expression, a reduced number of Ml macrophages, a deficient phagocytic activity, and the prolongation of the permanence of inflammatory cells, lead to deficient muscle regeneration. The expression of TGF{beta}1 and the consequent accumulation of collagen in the muscle, likely contribute to the fibrosis observed 30 days after infection. These results provide new information on the pathogenesis of gas gangrene caused by C. perfringens, shed light on the basis of the poor muscle regenerative activity, and may open new perspectives for the development of novel therapies for patients suffering this disease.