Author/Authors :
Haastrup، نويسنده , , Eva and Bukh، نويسنده , , Jens Drachmann and Bock، نويسنده , , Camilla and Vinberg، نويسنده , , Maj and Thّrner، نويسنده , , Lise Wegner and Hansen، نويسنده , , Thomas and Werge، نويسنده , , Thomas and Kessing، نويسنده , , Lars Vedel and Ullum، نويسنده , , Henrik، نويسنده ,
Abstract :
Background
sion is accompanied by an inflammatory reaction and activation of cell mediated immunity (CMI) and stressors may induce the cytokine network in humans. The proinflammatory cytokine interleukin-18 (IL-18) is less investigated in depression but highly relevant since it is produced by activated macrophages and expressed in the brain.
s
stribution of six polymorphisms in IL10, IL18 and NF was compared between patients with a single episode of depression either preceded by a stressful life event (n = 182), or occurring without a prior stressful life event (n = 106) and a group of healthy control individuals (n = 335).
s
jor C allele of the IL18 rs187238 and the major G allele of rs1946518 had a significantly higher prevalence among the patients with a stressful life event prior to onset of disease than both patients without a stressful life event and compared with the healthy controls individuals. None of the examined IL10 or NF alleles were differently distributed among these groups.
tions
re nominally significant and not resistant to correction for multiple testing.
sion
jor C allele of the IL18 rs187238 and the major G allele rs1946518 have previously been associated with higher expression of IL-18 mRNA. Our data suggest that this genetic trend towards higher IL-18 production may increase the susceptibility to depression in response to stressful life events.
Keywords :
rs187238 , depression , stressful life events , IL18 , rs1946518