We are all in this together: Understanding organ crosstalk in the pathogenesis of acute respiratory distress syndrome
https://doi.org/10.1002/pul2.12418
Abstract
I am writing this as I return from a conference of over 10,000 professionals dedicated primarily to the research and clinical care of respiratory disease. It is wonderful to reconnect with friends, colleagues, and mentors; to network and form new professional relationships with like-minded researchers and clinicians; and to see all the wonderful work and scientific breakthroughs that are occurring in our field; but I cannot help but feel like this design is isolating and restrictive to our more lofty goals. In the manuscript by DeWolf and colleagues entitled, “Human pulmonary microvascular endothelial cells respond to damage-associated molecular patterns (DAMPs) from injured renal tubular cells” the authors identify important organ crosstalk with a molecular signal released from renal tubular cells that elicits endothelial activation and dysfunction in the lung.1 After necrotic injury to renal tubular epithelial cells, the authors identify numerous proteins released into the supernatant which are classified as DAMPs through their known interaction with NOD like receptors and toll like receptors. They show that these DAMPs activate important signaling pathways in lung microvascular endothelial cells, are associated with endothelial dysfunction, and cause increased endothelial barrier permeability. The authors conclude that lung microvascular endothelial cells respond to DAMPs derived from renal tubular epithelial cells during injury through pattern recognition receptors as a mechanism for crosstalk between the lung and kidney.