Abstract

Neutrophils serve as an active constituent of innate immunity and are endowed with distinct ability for producing neutrophil extracellular traps (NETs) to eliminate pathogens. Earlier studies have demonstrated a dysfunction of the innate immune system in diabetic subjects leading to increased susceptibility to infections; however, the influence of hyperglycemic conditions on NETs is unknown. In the present study we demonstrate that (a) NETs are influenced by glucose homeostasis, (b) IL-6 is a potent inducer of energy dependent NET formation and (c) hyperglycemia mimics a state of constitutively active pro-inflammatory condition in neutrophils leading to reduced response to external stimuli making diabetic subjects susceptible to infections.

Original languageEnglish
Pages (from-to)2241-2246
Number of pages6
JournalFEBS Letters
Volume587
Issue number14
DOIs
Publication statusPublished - 11-07-2013

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Immune system
Pathogens
Interleukin-6
Homeostasis
Glucose
Neutrophils
Infection
Innate Immunity
Hyperglycemia
Immune System
Extracellular Traps

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

Cite this

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title = "High glucose modulates IL-6 mediated immune homeostasis through impeding neutrophil extracellular trap formation",
abstract = "Neutrophils serve as an active constituent of innate immunity and are endowed with distinct ability for producing neutrophil extracellular traps (NETs) to eliminate pathogens. Earlier studies have demonstrated a dysfunction of the innate immune system in diabetic subjects leading to increased susceptibility to infections; however, the influence of hyperglycemic conditions on NETs is unknown. In the present study we demonstrate that (a) NETs are influenced by glucose homeostasis, (b) IL-6 is a potent inducer of energy dependent NET formation and (c) hyperglycemia mimics a state of constitutively active pro-inflammatory condition in neutrophils leading to reduced response to external stimuli making diabetic subjects susceptible to infections.",
author = "Joshi, {Manjunath B.} and Apurva Lad and {Bharath Prasad}, {Alevoor S.} and Aswath Balakrishnan and Lingadakai Ramachandra and Kapaettu Satyamoorthy",
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T1 - High glucose modulates IL-6 mediated immune homeostasis through impeding neutrophil extracellular trap formation

AU - Joshi, Manjunath B.

AU - Lad, Apurva

AU - Bharath Prasad, Alevoor S.

AU - Balakrishnan, Aswath

AU - Ramachandra, Lingadakai

AU - Satyamoorthy, Kapaettu

PY - 2013/7/11

Y1 - 2013/7/11

N2 - Neutrophils serve as an active constituent of innate immunity and are endowed with distinct ability for producing neutrophil extracellular traps (NETs) to eliminate pathogens. Earlier studies have demonstrated a dysfunction of the innate immune system in diabetic subjects leading to increased susceptibility to infections; however, the influence of hyperglycemic conditions on NETs is unknown. In the present study we demonstrate that (a) NETs are influenced by glucose homeostasis, (b) IL-6 is a potent inducer of energy dependent NET formation and (c) hyperglycemia mimics a state of constitutively active pro-inflammatory condition in neutrophils leading to reduced response to external stimuli making diabetic subjects susceptible to infections.

AB - Neutrophils serve as an active constituent of innate immunity and are endowed with distinct ability for producing neutrophil extracellular traps (NETs) to eliminate pathogens. Earlier studies have demonstrated a dysfunction of the innate immune system in diabetic subjects leading to increased susceptibility to infections; however, the influence of hyperglycemic conditions on NETs is unknown. In the present study we demonstrate that (a) NETs are influenced by glucose homeostasis, (b) IL-6 is a potent inducer of energy dependent NET formation and (c) hyperglycemia mimics a state of constitutively active pro-inflammatory condition in neutrophils leading to reduced response to external stimuli making diabetic subjects susceptible to infections.

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