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Intracellular ATP Decrease Mediates NLRP3 Inflammasome Activation upon Nigericin and Crystal Stimulation.

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Intracellular ATP (iATP) depletion triggers NLRP3 inflammasome activation and IL-1β secretion by causing mitochondrial dysfunction. Maintaining iATP levels may offer a strategy against NLRP3-mediated inflammatory diseases.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Biochemistry

Background:

  • The NLRP3 inflammasome is crucial for inflammatory responses and linked to diseases like gout and atherosclerosis.
  • While extracellular ATP is a known NLRP3 activator, the role of intracellular ATP (iATP) is not well understood.

Purpose of the Study:

  • To investigate the role of intracellular ATP (iATP) in NLRP3 inflammasome activation and IL-1β secretion.
  • To elucidate the mechanisms linking iATP levels to mitochondrial function and inflammation.

Main Methods:

  • Utilized activated macrophages treated with glycolysis inhibitors (2-deoxyglucose) to reduce iATP.
  • Administered known NLRP3 activators (nigericin, monosodium urate crystals) to assess iATP changes.
  • Monitored mitochondrial membrane potential and IL-1β secretion.

Main Results:

  • Artificial reduction of iATP induced mitochondrial depolarization, leading to NLRP3- and caspase-1-dependent IL-1β secretion.
  • NLRP3 activators decreased iATP levels via K(+)- and Ca(2+)-mediated mitochondrial dysfunction.
  • Identified a feedback loop where iATP loss exacerbates mitochondrial dysfunction.

Conclusions:

  • Intracellular ATP plays a fundamental role in maintaining mitochondrial function and regulating IL-1β secretion.
  • iATP depletion is a key driver of NLRP3 inflammasome activation.
  • Maintaining intracellular ATP pools could be a therapeutic strategy against NLRP3-mediated inflammation.