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  • br Methods br Results br Discussion The aim of


    Discussion The aim of this study was to investigate whether serum lectin-binding activity is associated with development of HCC in HCV-positive individuals. Using ELISA-based assays of lectin-binding activity, we demonstrated that both age and gender influence the circulating binding activity of MBL, ficolin-2 and ficolin-3 in healthy controls. Men consistently displayed lower binding activity of serum ficolin-2 and ficolin-3 than women at ages < 40 years but were comparable in donors greater than 40 years old. The pattern observed for MBL was less clear; while the expression levels did appear to have a small decline in older individuals, the spread of values obtained was much greater, with some donors having an MBL-deficient phenotype. These data are consistent with reports that MBL expression declines in older healthy Chinese individuals (Ip et al., 2004) and that ficolin-2 expression is influenced by pregnancy (Halmos et al., 2012). It is important to note that genetic polymorphisms, several of which are linked to ethnicity, influence PRR expression levels. While complete data on these factors was lacking, it is unlikely that demographic factors biased any one group in our study due to the comparable ethnicities of the three groups. We did attempt to address the impact of polymorphisms on the expression of MBL in our HCV-infected patients. However, due to the nature of the samples collected, we were only able to determine promoter genotypes for a small subset of the cases. The descriptive statistics produced suggested that polymorphisms do not account for the differences in MBL activity observed between HCV-infected patients with, or without, HCC. The observation that HCV-infected patients with HCC had higher levels of MBL and ficolin-2 activity than those without HCC is consistent with a mechanism of fibrosis/disease progression controlled by MASP activation of stellate STF 31 mg (Saeed et al., 2013). Interestingly, this increase in lectin levels is in contrast to a previous study measuring total lectin concentration (rather than binding activity) that observed reduced ficolin-2 serum concentrations in patients with HCC following HBV infection (Hoang et al., 2011). This suggests that these two chronic hepatotropic viruses may cause liver cancer by distinct mechanisms, affecting liver-expressed PRRs to different extents. Serum concentrations of ficolin-2 and ficolin-3 are increased in ovarian cancer (Szala et al., 2013). However, in all these cancers it remains to be determined whether the altered expression of ficolins is causal, or a result of the growth of tumour tissue. The assays used in this study measured the functional binding of PRRs to their ligands, compared to reference samples. Non-synonymous polymorphisms in the PRR coding regions may alter binding to ligands. Assessing the activity of serum lectins in this way provides the most accurate comparison of binding activity present in serum. The estimated serum concentrations of the three PRRs were broadly similar to that observed in previous studies (data not shown), with the elevated levels of ficolin-2 being comparable to those observed in patients with ovarian cancer (Szala et al., 2013).
    Acknowledgements This study was funded by a split-site Ph.D. scholarship between the University of Sulaimani and University of Nottingham.
    Introduction Hepatitis C virus (HCV) is a ribonucleic acid (RNA) virus which may lead to liver inflammation, liver cirrhosis and hepatocellular carcinoma (HCC) (Hwang and Lee, 2011). HCV infection affects about a quarter billion people worldwide, and of those approximately 80% develops chronic hepatitis C infection (CHC). Further, in 20–30% of the persons with CHC infection may be occur cirrhosis and HCC (Hwang, 2001). HCV genotype 1 is more prevalent among the infected individuals with HCV, and its response to treatment is very hardly (Magri et al., 2017). Hepatic steatosis is known as accumulation of lipid molecules in hepatocytes, and which is a histological characteristic of CHC infection (Zampino et al., 2008), and its prevalence is approximately 55% in CHC infection (Lonardo et al., 2006). Hepatic steatosis in CHC infection is depending on metabolic and viral factors; obesity, insulin resistance (IR), diabetes mellitus (DM), hyperlipidemia and HCV genotypes, viral load, HCV core protein, respectively (Moriya et al., 1997; Barba et al., 1997).