Gout is now the most common cause of inflammatory arthritis, and its epidemiology worldwide points to an increase in incidence and prevalence in both developed and developing countries, Gout is caused by hyperuricaemia leading to the formation and deposition of monosodium urate (MSU) crystals. Gout is now regarded as a prototypical inflammatory disease driven by activation of the innate immune system.
• Inflammatory cytokines, in particular IL?1β, are the key mediators of gouty inflammation.
• The NLRP3 inflammasome is the major pathway by which MSU crystals trigger the cellular inflammatory response.
• Multiple regulatory pathways modulate the activity of the inflammasome and the release of IL?1β; this may explain in part the clinical origins of gouty inflammation, Once activated, IL­1R1 and its co­receptor IL­1 receptor accessory protein (IL­1RAcP) recruit a signalling complex that shares components with TLR signalling pathways, leading to the activation of pro-inflammatory transcription factors including nuclear factor­κB (NF­κB) as well as p38 c­Jun N­terminal kinase (JNK).
• Diet influences hyperuricaemia as well as the inflammatory state of macrophages in gout.
• Nutrients can modulate inflammasome activity and IL?1β release and participate in the regulation of pro-inflammatory as well as anti-inflammatory pathways in gout.

References

1.So AK and Martinon F. Nat Rev Rheumatol. 2017;13(11):639–647.