TY - JOUR
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.
UR - http://www.scopus.com/inward/record.url?scp=84879692964&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84879692964&partnerID=8YFLogxK
U2 - 10.1016/j.febslet.2013.05.053
DO - 10.1016/j.febslet.2013.05.053
M3 - Article
C2 - 23735697
AN - SCOPUS:84879692964
SN - 0014-5793
VL - 587
SP - 2241
EP - 2246
JO - FEBS Letters
JF - FEBS Letters
IS - 14
ER -
