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Increased Levels of AIM2 and Circulating Mitochondrial DNA in Type 2 Diabetes

Yolanda Guadalupe Cataño Cañizales1, Edith Elena Uresti Rivera, Rocío Edith García Jacobo

  • 1Medical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.

Iranian Journal of Immunology : IJI
|June 28, 2018
PubMed
Abstract

Insights

AIM2 and mitochondrial DNA (mtDNA) are involved in chronic inflammation in Type 2 diabetes (T2D). Increased AIM2 expression and mtDNA levels were observed in T2D patients, suggesting their role in the disease's inflammatory processes.

Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • Chronic inflammation plays a key role in Type 2 diabetes (T2D) pathogenesis.
  • Interleukin-1 beta (IL-1β) contributes to insulin resistance and beta-cell dysfunction in T2D.
  • Activation of inflammasomes like NLRP3 and AIM2 by endogenous ligands, such as mitochondrial DNA (mtDNA), can trigger IL-1β release.

Purpose of the Study:

  • To investigate the expression and activation of AIM2 inflammasome.
  • To quantify circulating mitochondrial DNA (mtDNA) levels in patients with T2D.
  • To explore the association between AIM2, mtDNA, and T2D clinical parameters.

Main Methods:

  • AIM2 expression was quantified using flow cytometry.
  • AIM2 activation was assessed by measuring IL-1β release in vitro.
  • mtDNA copy number was determined by quantitative real-time polymerase chain reaction (qPCR).

Main Results:

  • T2D patients exhibited increased AIM2-positive cells in monocytes and elevated IL-1β levels.
  • Higher mtDNA copy numbers were found in T2D patients compared to healthy controls.
  • AIM2+ cells correlated with hyperglycemia, triglycerides, and waist-hip ratio; mtDNA copy number correlated with BMI and TNF-α levels.

Conclusions:

  • The findings indicate a significant involvement of AIM2 inflammasome and mtDNA in the inflammatory pathways of T2D.
  • AIM2 and mtDNA may serve as potential biomarkers or therapeutic targets in T2D management.
  • Further research is warranted to elucidate the precise mechanisms linking AIM2, mtDNA, and T2D pathophysiology.

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