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Where next for cell-based therapy in ARDS
  1. Andrew James Boyle1,2,
  2. Cecilia M O’Kane1,
  3. Daniel Francis McAuley1,2
  1. 1 Centre for Experimental Medicine, Queen’s University Belfast, Belfast, UK
  2. 2 Regional Intensive Care Unit, Royal Victoria Hospital, Belfast, UK
  1. Correspondence to Dr Daniel Francis McAuley, Centre for Experimental Medicine, Queen’s University Belfast, Belfast BT9 7BL, UK; d.f.mcauley{at}

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Acute respiratory distress syndrome (ARDS) is a form of acute hypoxaemic respiratory failure that is characterised by non-cardiogenic pulmonary oedema which occurs as a consequence of the breakdown of the alveolar–capillary unit.1 ARDS impacts more than 10% of all intensive care unit admissions, and pneumonia is the most common risk factor for ARDS.2 Current standard of care aims to minimise iatrogenic lung injury from mechanical ventilation,3 4 while clinical trials of pharmacological therapies that have targeted the underlying mechanisms driving the development of ARDS have failed to show benefit.5

Beyond pharmacological therapies, much interest in this field has focused on mesenchymal stromal cells (MSCs) as a potential therapeutic option for ARDS.6 In the latest development towards a cell-based therapy for ARDS, Park et al report the use of an human ex vivo lung perfusion model of ARDS to investigate MSC-derived microvesicles (MVs) as a therapy for ARDS.7 MSCs are pluripotent cells that can be extracted from various sources including bone marrow, adipose tissue and umbilical cord. In ARDS they may represent an attractive therapy because of a broad range of potentially beneficial effects, including anti-inflammatory, pro-reparative and antimicrobial effects.8–10 Excessive host inflammation contributes to alveolar epithelial and capillary endothelial damage, and in this setting MSCs have immunomodulatory effects via the secretion of several anti-inflammatory compounds including Interleukin (IL) 10 and IL1 receptor antagonist. Loss of alveolar fluid clearance (AFC) in patients with ARDS contributes to alveolar flooding and is associated with increased hospital mortality.11 The delivery of MSCs to injured lungs restored AFC in a human ex vivo model of lung injury. This effect was in-part mediated by the secretion of keratinocyte growth factor (KGF), one of several soluble growth factors produced by MSCs.12 Approximately …

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