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Ischaemia reperfusion injury at the time of lung transplantation may lead to primary graft dysfunction (PGD).1 Occurring within the first 72 hours following allograft reperfusion, PGD is characterised by hypoxaemia and alveolar infiltrates in the transplanted organ and occurs in up to 30% of patients.2 The development of PGD carries significant early mortality of up to 50% in 30 days.3 Those who survive the early postoperative period have a higher propensity to develop bronchiolitis obliterans syndrome,4 and long-term mortality is also higher at 1, 5 and 10 years.5
Several risk factors have been identified for the development of PGD, including a donor history of smoking, higher FiO2 at the time of reperfusion, elevated pulmonary arterial pressures, large volume blood transfusion and raised recipient body mass index.6 This observation has led to the development of ex vivo lung perfusion. Here. lungs are ventilated and perfused with an acellular buffer. The use of this technique has allowed longer total ischaemic time prior to transplantation without an increase in incidence of PGD.7 However, incomplete understanding of the immune mechanisms leading to ischaemia reperfusion injury is a major limitation to preventing disease onset. There are no disease-specific therapeutics available for the condition, nor to prevent progression to PGD. Improved understanding of the immune responses underlying ischaemia reperfusion injury may allow development of new therapeutic strategies.
Dysregulation of the innate immune response is central to ischaemia reperfusion pathobiology. Neutrophils …
Contributors Both authors contributed to writing this editorial and approved the final version.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
Author note CAL is an academic clinical lecturer supported by the National Institute for Health Research.
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