Establishing a macrophage model of inflammasome activation under conditions mimicking sepsis to characterise the effects of melatonin

Elena Musatti, Helen F. Galley, Nigel Webster

Research output: Contribution to journalAbstractpeer-review

Abstract

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated inflammatory host response to infection. Melatonin has antioxidant and anti-inflammatory activity and is currently under trial as a treatment for sepsis. The inflammasome is a cytosolic protein complex that intensifies inflammation in response to signals pathogen- and danger-associated molecular patterns, extracellular adenosine 5′-triphosphate (ATP), metabolic dysfunction, K+ efflux, and mitochondrial DNA. Once active, the inflammasome triggers caspase-1-dependent maturation of interleukin (IL)-1β, an important pro-inflammatory cytokine. Nigericin is a polyether ionophore which catalyses exchange of K+. The aim of this study was to develop an inflammasome activation model in macrophages under conditions mimicking sepsis using nigericin as a specific activator, in order to determine the effects of melatonin. In this study we describe the characterisation of the model.
Original languageEnglish
Pages (from-to)E496
Number of pages1
JournalBritish Journal of Anaesthesia
Volume123
Issue number4
Early online date13 Sept 2019
DOIs
Publication statusPublished - Oct 2019
EventBJA Research Forum - London
Duration: 8 May 20199 May 2019

Bibliographical note

Acknowledgements: We acknowledge the support of the BJA/RCoA for a PhD studentship for Elena Musatti.

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