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Updated: Dec 10, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Mechanisms of NLRP3 priming in inflammaging and age related diseases
Anna Gritsenko1, Jack P Green2, David Brough2
1Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Abstract:
The NLRP3 inflammasome is a vital part of the innate immune response, whilst its aberrant activation drives the progression of a number of non-communicable diseases. Thus, NLRP3 inflammasome assembly must be tightly controlled at several checkpoints. The priming step of NLRP3 inflammasome activation is associated with increased NLRP3 gene expression, as well as post-translational modifications that control NLRP3 levels and licence the NLRP3 protein for inflammasome assembly. Increasing life expectancy in modern society is accompanied by a growing percentage of elderly individuals. The process of aging is associated with chronic inflammation that drives and/or worsens a range of age related non-communicable conditions. The NLRP3 inflammasome is known to contribute to pathological inflammation in many settings, but the mechanisms that prime NLRP3 for activation throughout aging and related co-morbidities have not been extensively reviewed. Here we dissect the biochemical changes that occur during aging and the pathogenesis of age related diseases and analyse the mechanisms by which they prime the NLRP3 inflammasome, thus exacerbating inflammation.
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