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Spontaneous PMN apoptosis in type 2 diabetes and the impact of periodontitis

Aggasit Manosudprasit1, Alpdogan Kantarci1, Hatice Hasturk2

  • 1Department of Applied Oral Sciences, The Forsyth Institute, Cambridge, Massachusetts, USA akantarci@forsyth.org.

Journal of Leukocyte Biology
|October 13, 2017
PubMed

Insights

Peripheral blood neutrophils (PMN) show delayed apoptosis in type 2 diabetes (T2DM) and chronic periodontitis (CP), with reduced caspase activity. This delay is linked to advanced glycation endproducts and RAGE signaling.

Area of Science:

  • Immunology
  • Endocrinology
  • Periodontology

Background:

  • Neutrophil apoptosis is a critical process in resolving inflammation.
  • Type 2 diabetes mellitus (T2DM) and chronic periodontitis (CP) are inflammatory conditions.
  • The interplay between T2DM, CP, and neutrophil function remains incompletely understood.

Purpose of the Study:

  • To investigate if peripheral blood neutrophils (PMN) exhibit delayed spontaneous apoptosis in individuals with T2DM.
  • To determine if this delay is exacerbated in individuals with coexisting T2DM and CP.
  • To explore the underlying molecular mechanisms involving caspases, death receptors, and advanced glycation endproducts (AGEs).

Main Methods:

  • Flow cytometry (TUNEL and Annexin V assays) to measure PMN apoptosis.
  • Colorimetric assays to quantify caspase-3, -8, and -9 activity.
  • Flow cytometry and multiplex immunoassays to analyze death receptor expression (TNFR1, FasR) and serum levels of Fas ligand (FasL).

Main Results:

  • Spontaneous PMN apoptosis was significantly reduced in individuals with T2DM, CP, and T2DM + CP compared to healthy controls.
  • Caspase-3 activity was decreased in T2DM and T2DM + CP groups.
  • Caspase-8 activity reduction was observed in CP and T2DM + CP groups, correlated with lower FasR, TNFRs, and FasL levels. AGEs/RAGE interaction induced PMN apoptosis.

Conclusions:

  • Delayed PMN apoptosis is a characteristic feature in individuals with T2DM and CP.
  • The observed inhibition of PMN apoptosis in T2DM is mediated by an advanced glycation endproducts/receptor for advanced glycation endproducts (AGEs/RAGE) pathway.
  • These findings highlight a potential mechanism linking metabolic and periodontal diseases through altered neutrophil function.
Keywords:
cell deathchronic inflammationleukocyte

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