Before LPS intervention, the TLR4, TNF-α, IL-1, and IL-6 levels were higher and the level of miR-155, IL-10 was lower in the ACS group compared with the SAP, CSF, and HC groups.
In the healthy control cohort, the associations with VWF and sTF were similar to those in ACS patients (P = 1.2 × 10-15 and P = 1.0 × 10-5 respectively), but the healthy cohort showed no association with IL-10 levels (P>0.05).
The ACS phenotype in this model correlated with deregulated expression of a number of cytokines, including elevated levels of interleukin-10 which was under the direct translational control of mTOR.
The polymorphisms at -308G→A of TNF-α, -174G→C of IL-6, +874A→T of IFN-γ and -1082G→A, and -592C→A of IL-10 genes evaluated in the present study are important risk factors for the development of ACS in the South Indian population from Andhra Pradesh.
While the functional attributes of these microsatellite markers remain to be seen, it is likely that they have distinct functional properties (altered IL-10 secretion), which in turn affect the susceptibility to ACS development.
Multiple logistic analyses by gender showed that male individuals with IL-10-592CC+AC genotypes had 3.54-fold increased risk of developing ACS than individuals with AA genotype (p<0.001).
In contrast with some previous reports, we conclude that IL-10 reflects a proinflammatory state in patients with ACS and we therefore suggest that IL-10 is as effective a biomarker for the risk prediction of future cardiovascular events as other markers of systemic inflammation.
Analysis of covariance showed that genetic variation in the apoE gene locus significantly influences serum IL-10 levels in both ACS (p = 0.009) and CSA patients (p = 0.013).