Near infrared light reduces neutrophil chemokine production during ischemia-reperfusion injury

Abstract

Abstract Background: Ischemia reperfusion injury and tissue necrosis commonly follows administration of a tourniquet. Previously, we have shown that exposure to non-thermal infrared (NIR) light decreases neutrophil and macrophage mediated inflammation and tissue necrosis in a mouse hindlimb model. This study tests whether exposure to NIR light during a period of ischemia limits tissue damage by reducing secretion of chemoattractant proteins and phenotypic switching of tissue macrophages from a pro-inflammatory (M1) to a wound healing (M2) phenotype. Methods and Results: Mouse hindlimbs received 3 hours of tourniquet-induced ischemia followed by a period of reperfusion with or without 15 or 30 minutes of NIR exposure. Hindlimbs receiving injury and NIR treatment showed a significant decrease in the neutrophil chemoattractants CXCL1 and CXCL5 by ELISA, compared with mice receiving ischemia reperfusion injury alone and control mice receiving no injury or NIR. Protein isolated from mouse hindlimbs receiving NIR treatment and injury had a significant decrease in M1 macrophage marker CD68 and significant increase in M2 macrophage marker CD206, normalized to CD14, compared with mice receiving injury alone and uninjured mice. Conclusion: We have shown that NIR light affects neutrophil chemokine secretion and tissue macrophage polarization in a murine hindlimb ischemia and reperfusion model. These data indicate that NIR light treatment during tourniquet administration limits inflammatory responses, reduces tissue necrosis, and promotes wound healing following removal of the tourniquet. Thus, NIR treatment may improve limb preservation following vascular injury and inform timing of tourniquet application during surgical procedures.