• Dominic Anthony Friston, Joshua Cuddihy, Jessica Souza Luiz, An Hoai Truong, Laptin Ho, Meirvaan Basra, Peter Santha, Orsolya Oszlacs, Joao de Sousa Valente, Tim Marczylo, Sini Junttila, Helen Laycock, Declan Collins, Marcela Vizcaychipi, Attila Gyenesei, Zoltan Takats, Gabor Jancso, Elizabeth Want, and Istvan Nagy.
• Nociception Group, Division of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
• Pain. 2023 Feb 1; 164 (2): e103e115e103-e115.

AbstractTissue injuries, including burns, are major causes of death and morbidity worldwide. These injuries result in the release of intracellular molecules and subsequent inflammatory reactions, changing the tissues' chemical milieu and leading to the development of persistent pain through activating pain-sensing primary sensory neurons. However, the majority of pain-inducing agents in injured tissues are unknown. Here, we report that, amongst other important metabolite changes, lysophosphatidylcholines (LPCs) including 18:0 LPC exhibit significant and consistent local burn injury-induced changes in concentration. 18:0 LPC induces immediate pain and the development of hypersensitivities to mechanical and heat stimuli through molecules including the transient receptor potential ion channel, vanilloid subfamily, member 1, and member 2 at least partly via increasing lateral pressure in the membrane. As levels of LPCs including 18:0 LPC increase in other tissue injuries, our data reveal a novel role for these lipids in injury-associated pain. These findings have high potential to improve patient care.Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.

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