Abstract
Macrophages play a very important role in the conduction of several regenerative processes mainly due to their plasticity and multiple functions. In the muscle repair process, while M1 macrophages regulate the inflammatory and proliferative phases, M2 (anti‐inflammatory) macrophages direct the differentiation and remodelling phases, leading to tissue regeneration. The aim of this study was to evaluate the effect of red and near infrared (NIR) photobiomodulation (PBM) on macrophage phenotypes and correlate these findings with the repair process following acute muscle injury. Wistar rats were divided into 4 groups: control; muscle injury; muscle injury + red PBM; and muscle injury + NIR PBM. After 2, 4 and 7 days, the tibialis anterior muscle was processed for analysis. Macrophages phenotypic profile was evaluated by immunohistochemistry and correlated with the different stages of the skeletal muscle repair by the qualitative and quantitative morphological analysis as well as by the evaluation of IL‐6,TNF‐α and TGF‐β mRNA expression. Photobiomodulation at both wavelengths was able to decrease the number of CD68+ (M1) macrophages 2 days after muscle injury and increase the number of CD163+ (M2) macrophages 7 days after injury. However, only NIR treatment was able to increase the number of CD206+ M2 macrophages (Day 2) and TGF ‐β mRNA expression (Day 2, 4 and 7), favouring the repair process more expressivelly. Treatment with PBM was able to modulate the inflammation phase, optimize the transition from the inflammatory to the regeneration phase (mainly with NIR light) and improve the final step of regeneration, enhancing tissue repair.
Highlights
Acute muscle injuries provide a good model for the study of the modulating effect of immune cells on the tissue repair process.[1]
Macrophages constitute the majority of intramuscular leucocytes and, besides removing tissue debris through phagocytosis, these cells synthesize growth factors, chemokines and cytokines that modulate all phases of muscle repair.[1,2]
Under the microenvironment stimuli provided mainly by infiltrated neutrophils in the initial steps after an acute muscle injury, macrophages are activated and acquire a proinflammatory phenotype, classically known as M1 (CD68high, CD206− and CD163−) and characterized by enhanced phagocytic activity and production of proinflammatory mediators as IL‐1β, IL‐6, TNF‐α, IL‐12 and IL‐23.1,3-5 Other mediators released by M1 macrophages, such as IL‐6, IL‐1, VEGF and IL‐13, stimulate angiogenesis and the proliferation of myogenic precursor cells.[1,4,5]
Summary
Acute muscle injuries provide a good model for the study of the modulating effect of immune cells on the tissue repair process.[1]. After an acute injury, muscle tissue undergoes the rapid invasion of inflammatory cells, mainly neutrophils and macrophages.[1]. Macrophages constitute the majority of intramuscular leucocytes and, besides removing tissue debris through phagocytosis, these cells synthesize growth factors, chemokines and cytokines that modulate all phases of muscle repair.[1,2]. Under the microenvironment stimuli provided mainly by infiltrated neutrophils (ie, presence of Th1 mediators, such as IFN-γ and TNF-α) in the initial steps after an acute muscle injury, macrophages are activated and acquire a proinflammatory phenotype, classically known as M1 (CD68high, CD206− and CD163−) and characterized by enhanced phagocytic activity and production of proinflammatory mediators as IL‐1β, IL‐6, TNF‐α, IL‐12 and IL‐23.1,3-5 Other mediators released by M1 macrophages, such as IL‐6, IL‐1, VEGF and IL‐13, stimulate angiogenesis and the proliferation of myogenic precursor cells.[1,4,5]. Normal muscle tissue does not express CD68+ macrophages.[3,4]
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