Premium
Hepatitis B core antigen can regulate NLRP3 inflammasome pathway in HepG2 cells
Author(s) -
Ding Xiaolin,
Lei Qingsong,
Li Tianju,
Li Lin,
Qin Bo
Publication year - 2019
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.25490
Subject(s) - hbcag , hbeag , inflammasome , hepatitis b virus , virology , antigen , microbiology and biotechnology , biology , chemistry , hbsag , virus , immunology , inflammation
Hepatitis B virus (HBV) has four open reading frames (ORFs) of which ORF C is consists of the pre Core and Core genes encodes the Hepatitis B core antigen (HBcAg) and Hepatitis B e antigen (HBeAg). Studies have shown that HBeAg significantly inhibits the NLRP3 inflammasome activation and interleukin‐1β (IL‐1β) production. However, the role of HBcAg and ORF C proteins (in this paper, ORF C proteins = HBcAg + HBeAg) were remain unclear. Our study aims to assess whether HBcAg and ORF C proteins can affect the NLRP3 inflammasome pathway. Vectors expressing ORF C proteins and HBcAg were designed and transfected into HepG2 cells. And then, cells were stimulated with lipopolysaccharide (LPS). Activation of the NLRP3 inflammasome and the levels of IL‐1β and IL‐18 were evaluated by Western blot analysis, quantitative reverse‐transcription polymerase chain reaction, enzyme‐linked immunosorbent assay, and immunofluorescence. The expression of NLRP3 and IL‐1β peaked when HepG2 cells were stimulated with 1000 ng/mL LPS for 18 to 24 hours. HBcAg, but not ORF C proteins, promoted LPS‐induced NLRP3 inflammasome activation and IL‐1β production. These findings provide a novel mechanism on how the HBV causes liver inflammation and may provide insights into the search for new therapeutic strategies.