Can NLRP3 gene polymorphism in Egyptian chronic hepatitis C patients affect the degree of liver fibrosis?

Abstract

Background: The cytokines genes polymorphisms are important determinants for the outcome of HCV infection and degree of liver fibrosis and inflammation. Recently, it has been revealed that hepatocytes and hepatic macrophages produce mature IL-1β through the NLRP3 (NOD-like receptor, pyrin domain containing 3) inflammasome assembly which represents a link between hepatitis C virus infection and liver inflammation. In addition, NLRP3 inflammasome has emerged as a cytoplasmic sensor of HCV participating in eliciting the innate immune response against HCV. Objective: To explore the association of a genetic variation within 3’UTR NLRP3 gene with the degree of liver fibrosis and /or liver inflammation. Moreover, to investigate possible relation between fibrosis and the HCV load quantified at the diagnosis of Egyptian HCV patients. Methods: We studied the distribution of genotypes and alleles of one NLRP3 SNP (rs10754558) in one hundredforty seven chronic HCV patients using Taq Man predesigned SNP genotyping assay. Results: The genotype distribution and allele frequencies of NLRP3 (rs10754558) polymorphism did not differ significantly neither with the degree of liver fibrosis nor with the degree of liver inflammation or the baseline HCV quantity. Conclusions: NLRP3 (rs10754558) polymorphism was not associated neither with the degree of liver fibrosis nor with the degree of liver inflammation and amplitude of baseline HCV load measured during diagnosis of Egyptian patients chronically infected with HCV genotype 4a. Importantly, the pivotal role played by the NLRP3 in the immune response against HCV infection requires further studies for other polymorphisms within NLRP3 gene to unravel their role in HCV infection.