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α ‐Defensin increase in peripheral blood mononuclear cells from patients with hepatitis C virus chronic infection
Author(s) -
Aceti A.,
Mangoni M. L.,
Pasquazzi C.,
Fiocco D.,
Marangi M.,
Miele R.,
Zechini B.,
Borro M.,
Versace I.,
Simmaco M.
Publication year - 2006
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2006.00762.x
Subject(s) - defensin , peripheral blood mononuclear cell , nfat , immunology , hepatitis c virus , medicine , hepatitis b virus , hepatitis c , fibrosis , hepatitis , biology , virology , virus , gene , in vitro , transplantation , calcineurin , biochemistry
Summary. The α ‐defensin genes promoter regions contain a putative nuclear factors of activated T cells (NFAT)‐binding site and it is known that hepatitis C virus (HCV) core protein activates the interleukin (IL)‐2 gene transcription through the NFAT pathway. The aims of this study were to investigate if HCV affects the α ‐defensin expression in peripheral human mononuclear cells (PBMCs) and to evaluate the existence of a correlation between α ‐defensins and liver damage in patients with chronic hepatitis C. Ninety patients with chronic hepatitis C, 30 with chronic hepatitis B and 25 healthy controls were enrolled. α ‐Defensins were identified and quantified in PBMCs by mass spectrometry, enzyme‐linked immunosorbent assay, antibacterial activity and mRNA levels. PBMCs from three patients and controls were stimulated with HCV core protein, hepatitis B virus core antigen and the α ‐defensin mRNAs level was quantified. We found that HCV core protein activates in vitro the α ‐defensin transcription. α ‐Defensin levels in patients with chronic hepatitis C (mean ± SD = 1.103 ± 0.765 ng/10 6 cells), chronic hepatitis B (0.53 ± 0.15) and healthy controls (0.217 ± 0.09) resulted significantly different ( P < 0.001). In patients with chronic hepatitis C, the α ‐defensin levels and antibacterial activity correlate with the liver fibrosis. Our data suggest that HCV induces α ‐defensin expression. The high linear correlation of α ‐defensin levels with advancing fibrosis makes the measure of these peptides a reliable marker to evaluate fibrosis stage.