CX3CR1 and acute respiratory distress syndrome: <i>In vitro</i>, PBM dose-dependently suppressed LPS-induced TNF-α/IL-6 and IL-1β while increasing IL-10, restored ATP, reduced mitochondrial ROS, and improved membrane potential, that benefits lost with AdipoR1 silencing.<h4>Conclusions</h4>Septic ALI modulated by 650 nm PBM was characterized by suppressing CCR2<sup>+</sup> inflammatory recruitment, enriching CX3CR1<sup>+</sup>/M2-like macrophages, and preserving mitochondrial function through adiponectin-AdipoR1 signaling.