MACROPHAGE-DERIVED SUPEROXIDE PRODUCTION AND ANTIOXIDANT RESPONSE FOLLOWING SKELETAL MUSCLE INJURY

Publication date: Available online 17 February 2018
Source:Free Radical Biology and Medicine
Author(s): Emmeran Le Moal, Gaëtan Juban, Anne Sophie Bernard, Tamas Varga, Clotilde Policar, Bénédicte Chazaud, Rémi Mounier
Macrophages are key players of immunity that display different functions according to their activation states. In a regenerative context, pro-inflammatory macrophages (Ly6C^pos) are involved in the mounting of the inflammatory response whereas anti-inflammatory macrophages (Ly6C^neg) dampen the inflammation and promote tissue repair. Reactive oxygen species (ROS) production is a hallmark of tissue injury and of subsequent inflammation as described in a bacterial challenge context. However, whether macrophages produce ROS following a sterile tissue injury is uncertain. In this study, we used complementary in vitro, ex vivo and in vivo experiments in mouse to show that macrophages do not release ROS following a sterile injury in skeletal muscle. Furthermore, expression profiles of genes involved in the response to oxidative stress in Ly6C^pos and Ly6C^neg macrophage subsets did not indicate any antioxidant response in this context. Finally, in vivo, pharmacological antioxidant supplementation with N-Acetyl-cysteine (NAC) following skeletal muscle injury did not alter macrophage phenotype during skeletal muscle regeneration. Overall, these results indicate that following a sterile injury, macrophage-derived ROS release is not involved in the regulation of the inflammatory response in the regenerating skeletal muscle.

Graphical abstract

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