A study published in Hepatology provides new insights into genetic variations of pro-inflammatory citokines and how these may influence the intensity of systemic inflammation in patients with acutely decompensated cirrhosis. Because of their association with inflammation-related genes, six single-nucleotide polymorphism (SNPs) were considered. The six SNPs of interest were genotyped in 279 patients with cirrhosis with (n = 178) and without (n = 101) ACLF from the CANONIC study. Among these SNPs, only those related to IL-1 beta and IL-1 receptor agonist (IL-1ra) were strongly associated with ACLF.
Researchers found that the two “protective” SNPs are located on chromosome 2 in the region of the IL-1 gene cluster. Thus, SNPs at the IL-1 locus could represent quantitative trait loci (QTLs) that impact cytokine gene expression. Since the IL-1 locus exhibits a large number of SNPs, future studies should address whether the two SNPs identified in this study are actually lead SNPs or are “overcome” by other SNP(s) at the same locus with respect to their association to the level of circulating cytokines in patients with acute decompensation of cirrhosis.
These results will guide future investigations with the aim to identify crucial QTLs that drive the intensity of cytokine production and the subsequent risk of organ failure. Future research carried out under the umbrella of the Grifols Chair for Translational Research will combine genome-wide association studies and transcriptome analyses or assessment of circulating levels of a large number of cytokines and chemokines. These studies will allow us to further understand whether the QTLs associated to intensity of inflammation are dependent on the nature of stimuli or not, and shed some new light on the mechanisms that drive the progression of cirrhosis towards very severe stages of the disease.
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