Abstract
The transition between the inflammatory phase and the proliferative phase is critical for wound healing. However, the development of proper switchers that can regulate this transition is facing great challenges. Macrophages play versatile roles in all wound healing phases because they can readily switch from pro-inflammatory M1 phenotypes to anti-inflammatory M2 phenotypes in response to different microenvironment stimuli. Herein, taking advantage of enhanced electron transfer by coupling MoS(2) with a highly conductive activated carbon fiber (ACF) network, a MoS(2)-ACF heterojunction structure was constructed as a macrophage M1-M2 phenotype switcher (MAPS) for regulating inflammation-proliferation transition to accelerate wound healing. In the early stages of wound repair, MAPS-mediated photothermal effects with near-infrared laser irradiation could promote macrophage reprogramming to the M1 phenotype, which can expedite inflammation. NIR photo-induced hyperthermia, together with M1 macrophages, directly and indirectly kills bacteria. Later, during the healing process, the MAPS could further reprogram macrophages towards the M2 phenotype via its inherent reactive oxygen species (ROS) scavenging ability to resolve inflammation, promoting cell proliferation. Therefore, MoS(2)-ACF heterojunction structures provide a new strategy to modulate inflammation-proliferation transition by rebalancing the immuno-environmental equilibrium of macrophage M1/M2 phenotypes.