The role of caloric load and mitochondrial homeostasis in the regulation of the NLRP3 inflammasome

Cell Mol Life Sci. 2017 May;74(10):1777-1791. doi: 10.1007/s00018-016-2431-7. Epub 2016 Dec 10.

Abstract

Sterile inflammation is a cornerstone of immune activation in obesity and type 2 Diabetes Mellitus. The molecular underpinnings of this inflammation include nutrient excess-mediated activation of the innate immune NLRP3 inflammasome. At the same time, disruption of mitochondrial integrity is emerging as an integral control node in NLRP3 inflammasome activation and is also associated with caloric overload conditions including obesity and diabetes. Conversely, caloric restriction and fasting mimetic interventions alleviate these caloric excess-linked diseases and reduce inflammation and the NLRP3 inflammasome. The objective of this review is to integrate the findings linking mitochondrial integrity to the activation of the NLRP3 inflammasome and to evaluate how caloric restriction or caloric restriction mimetic compounds may play a role in attenuating the NLRP3 inflammasome and sterile inflammation.

Keywords: Mitochondria; NLRP3 inflammasome; Obesity; Sirtuins; Sterile inflammation.

Publication types

  • Review
  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2 / immunology*
  • Diabetes Mellitus, Type 2 / pathology
  • Energy Intake
  • Humans
  • Inflammasomes / immunology*
  • Inflammation / immunology*
  • Inflammation / pathology
  • Mitochondria / immunology*
  • Mitochondria / pathology
  • NLR Family, Pyrin Domain-Containing 3 Protein / immunology*
  • Obesity / immunology*
  • Sirtuins / immunology

Substances

  • Inflammasomes
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • NLRP3 protein, human
  • Sirtuins