Fibrosis severity and mannan-binding lectin (MBL)/MBL-associated serine protease 1 (MASP-1) complex in HCV-infected patients.

BACKGROUND AND STUDY AIMS

Mannan-binding lectin (MBL) is a collectin synthesised in the liver and secreted into the bloodstream. It binds micro-organisms via interactions with glycans on the target surface. Bound MBL subsequently activates MBL-associated serine protease proenzymes (MASPs). Several studies have investigated the possible role for MBL in hepatitis C virus (HCV) infection by examining MBL levels and polymorphisms in relation to disease progression and in response to treatment. The aim of this study was to investigate the relation of the activity of MBL and MBL/MASP-1 complex in sera of patients with mild and severe chronic HCV infection and outcome of HCV infection.

PATIENTS AND METHODS

Serum level of MBL and functional assays for MBL/MASP-1 complex activity were assayed in sera of 80 patients with chronic HCV infection. Patients were divided into two groups according to the results of the liver biopsy, group I (40 HCV patients had mild hepatic fibrosis, Ishak fibrosis stages 0-1) and group II (40 HCV patients had severe hepatic fibrosis, Ishak fibrosis stages 5-6), in addition to 20 control subjects as group III. The analysis of the MBL/MASP-1 complex activity at 0, 3 and 6 months was performed in all patients.

RESULTS

Serum levels of MBL and MBL/MASP-1 complex activity were higher in sera of patients with chronic HCV liver disease compared to those in control subjects. There was a correlation between the activity of the MBL/MASP-1 complex and the severity of fibrosis (P=0.003). MBL/MASP-1 complex activity was associated more significantly with severe fibrosis in comparison to MBL concentration.

CONCLUSION

MBL and MBL/MASP-1 complex activities play a key role in first-line host defence mechanism against certain infectious agents including HCV infection. However, it is also likely that the role of MBL and MBL/MASP-1 complex activity extends beyond this restricted infection-related view in that it appears to be a key regulator of inflammation.