Serum ficolin-2 concentrations are significantly changed in patients with hepatitis B virus infection and liver diseases

Abstract

Human ficolin-2 is an important lectin complement pathway activator that is secreted from liver cells and has been implicated as an anti-infection innate immune molecule. However, the role of ficolin-2 protein and its dynamic changes over the course of and in the prognosis of chronic hepatitis B (CHB) and hepatocellular carcinoma (HCC) remain unclear. In this study, we analyzed ficolin-2 protein expression in a cohort of individuals with CHB infection, HCC and cirrhosis. A sandwich enzyme-linked immunosorbent assay (ELISA) method was used to measure serum ficolin-2 concentrations. Ficolin-2 expression in liver tissues was detected by immunohistochemical staining. Serum ficolin-2 concentrations in CHB patients were significantly higher than in healthy controls and HBV carriers. After 48 weeks of routine amelioration liver function treatment, serum ficolin-2 concentrations decreased and were positively correlated with favorable alanine aminotransferase (ALT), HBV DNA and HBeAg-seroconversion outcomes. Interestingly, we observed much lower expression of serum and intrahepatic ficolin-2 in HCC and cirrhosis compared with healthy controls. Our findings suggest that serum and intrahepatic ficolin-2 levels may be considered one of the indicators for the response of chronic HBV infection, HCC and cirrhosis.

Inflammatory biomarkers and cancer: CRP and suPAR as markers of incident cancer in patients with serious nonspecific symptoms and signs of cancer

“…13,14 Also, MBL concentration has been found to be increased in patients with colorectal cancer, 15 advanced ovarian cancer, 16 glioblastoma multiforme 17 and thyroid cancer. 11 On the contrary, serum and intrahepatic ficolin-2 levels have also been found to be decreased in patients with hepatocellular carcinoma compared to healthy persons, 44 and in children with cancer, serum ficolin-1 levels were not different from age-matched controls. 45 In our patient cohort, these PRRs did not add diagnostic information; pentraxin-3 was significantly higher in patients with cancer compared to patients with no abnormalities detected, but this association was not significant in the adjusted analyses.…”

The Lack of Association between <b><i>FCN2</i></b> Gene Promoter Region Polymorphisms and Dental Caries in Polish Children

“…Several studies investigated the association of FCN2 functional polymorphisms and/or ficolin-2 serum levels with different infectious diseases, including respiratory infections [Atkinson et al, 2004;Ruskamp et al, 2009], pneumonia [Chalmers et al, 2014], invasive pneumococcal disease [Chapman et al, 2007], pulmonary tuberculosis [Luo et al, 2013;Xu et al, 2015], leprosy [de MessiasReason et al, 2009;Zhang et al, 2013], hepatitis B [Hoang et al, 2011;Chen et al, 2015], leishmaniasis [Assaf et al, 2012;Mishra et al, 2015], schistosomiasis [Ouf et al, 2012] or autoimmune diseases with bacterial involvement, such as rheumatic fever and chronic rheumatic heart disease .…”

Ficolin‐A/2, acting as a new regulator of macrophage polarization, mediates the inflammatory response in experimental mouse colitis

“…Upon binding to their specific pathogen‐associated molecular patterns, FCNs may trigger the activation of the immune system either (i) by initiating the activation of complement via the lectin pathway, (ii) through a primitive type of opsonophagocytosis, or (iii) by stimulating the secretion of inflammatory cytokines by macrophages, so limiting the infection and concurrently orchestrating the subsequent adaptive immune response. Our and others' previous studies have indicated that FCN‐A/2 was an anti‐bacterial and anti‐viral innate immune molecule . In our present study, FCN‐A/2 played important pro‐inflammatory roles in the induction phase of acute colitis.…”

“…Recently, a number of reports have shown that the dysfunction or abnormal expression of FCN‐A/2 may play crucial roles in immune responses, inflammatory processes, viral and bacterial diseases . However, little is known regarding the roles and mechanisms of FCN‐A/2 in intestinal inflammation.…”