While the immune profiles in the different schizophrenia phenotypes indicate the activation of the immune-inflammatory response system (IRS), there are simultaneous signs of CIRS activation, including increased levels of the IL-1 receptor antagonist (sIL-1RA), sIL-2R and tumor necrosis factor-α receptors, Th-2 and Treg phenotypes with increased IL-4 and IL-10 production, and increased levels of TRYCATs and haptoglobin, α2-macroglobulin, and other acute-phase reactants, which have immune-regulatory and anti-inflammatory effects.
<b>Results:</b> Compared with the HC, peripheral IL-10 levels were higher and a significant reduction of FA and AD, and increase of RD and MD were observed in SZ (corrected <i>p</i> < 0.05).
Random-effect meta-analysis showed that increasing maternal CRP (OR = 1.31, 95% CI 1.11-1.55, SMD = 0.15, 95% CI 0.06-0.24, P < 0.01), pro-inflammatory cytokine interleukin (IL)-8 (OR = 1.64, 95% CI 1.06-2.55, SMD = 0.27, 95% CI 0.03-0.52, P = 0.03) and anti-inflammatory cytokine IL-10 (OR = 2.16, 95% CI 1.30-3.59, SMD = 0.43, 95% CI 0.14-0.71, P < 0.01) were significantly associated with schizophrenia in offspring.
The magnitude of increase in IL-1β, IL-6, IL-8 and IL-10 mRNAs in people in the elevated inflammation biotype ranged from 100 to 220% of those in the non-elevated inflammatory biotype and was comparable between control and schizophrenia groups.
We therefore examined the impact of possible correlation between IL-10 genetic variations and the plasma levels of soluble HLA-G (sHLA-G) on schizophrenia risk.
Relationships between messenger RNA (mRNA) expression of 11 schizophrenia-related genes and circulating levels of cytokines (interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α) were analyzed in 174 antipsychotic naïve first episode psychosis (FEP) and in 77 healthy controls.
An association of rs4848306 in IL1B gene, rs4251961 in IL1RN gene, rs2228145 and rs4537545 in IL6R with schizophrenia have been observed. rs6676671 in IL10 was associated with early age of onset.
Among which, the role of interleukin-10 (IL-10) in SZ has been explored in a number of studies by investigating association of single nucleotide polymorphisms (SNPs) and susceptibility of SZ.
No obvious interactions among the potential polymorphisms were found, which suggests that IL-10 and DRD4 confer vulnerability to schizophrenia independently.
On the basis of the evidence of the sex-dependent effect of certain genes in many complex diseases, we conducted a sex-stratified case-control association study to verify the linkage of the IL-10 gene promoter SNPs and haplotypes with schizophrenia and the possible sex-specific genetic effect in a Spanish schizophrenic population.
Polymorphisms at position -1082, -819 and-592 in the IL-10 promoter region were determined in 171 Turkish patients who were diagnosed with schizophrenia, based on the DSM-IV, and 168 healthy controls, by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP).
It has been established that cytokines play a critical role in the regulation of the CNS and recent studies have suggested that dysfunctions of both pro-inflammatory (IL-1beta, IL-6, and TNF-alpha) and anti-inflammatory (IL-1RA and IL-10) cytokines could be involved in the pathophysiology of schizophrenia.
These data could partly explain the abnormal secretion of IL-10 occurring in schizophrenic patients in response to infections or different stressors and suggest a potential role of IL-10 as a candidate gene for susceptibility to schizophrenia.
The present study suggests that IL-10 gene polymorphism at position -819 does not confer susceptibility to major depression and schizophrenia, at least in the Korean population.