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Although reduced tidal volumes have improved patient survival during ventilation for acute lung injury, further improvements will require pharmacologic interventions of the cellular pathways for inflammation and injury. We previously reported that pretreatment with mitochondrial targeted mtDNA repair enzymes largely prevented lung injury and inflammation during a protocol for moderately severe ventilation induced lung injury. GSH/GSSG ratios indicated that free radical production had been reduced to baseline levels by treatment. The central role of the alveolar macrophages and cellular mechanisms of injury are discussed. This includes a rapid calcium entry and mitochondrial production of excessive reactive oxygen species. Excessive ROS can then result in activation of the NLRP3 inflammasome and secretion of IL-1 and IL-18 by caspase-1. A simultaneous activation of NFkB to transcribe pro forms of the cytokines is stimulated by damage associated molecular pattern (DAMP) recognition receptors. These are primarily TLR4 responding to various cellular damage products and TLR9 responding to mtDNA fragments that appear to be primarily involved. Intervention in these pathways could result in useful future clinical treatments.

Mitochondrial damage pathways in ventilator induced lung injury (VILI): an update