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IFI16 induces inflammation in hepatitis B virus-associated glomerulonephritis by regulating the Caspase-1/ IL-1 ß

Li Liu1, Shuangshuang Xie1, Cheng Li1

  • 1Department of Liver Diseases, Shandong Public Health Clinical Center, Shandong University, Jinan, 250000, China.

Diagnostic Pathology
|April 23, 2022
PubMed
Abstract

Insights

IFI16, a key immune sensor, is elevated in Hepatitis B Virus-Associated Glomerulonephritis (HBV-GN) and promotes inflammation. This suggests IFI16 is a potential therapeutic target for HBV-GN pathogenesis.

Area of Science:

  • Immunology
  • Virology
  • Nephrology

Background:

  • Interferon gamma-induced protein 16 (IFI16) is crucial for innate immunity against double-stranded DNA viruses via inflammasome activation.
  • The specific role of IFI16 in Hepatitis B Virus-Associated Glomerulonephritis (HBV-GN) and its sensing of hepatitis B virus (HBV) remain unclear.

Purpose of the Study:

  • To investigate the inflammatory role of IFI16 in HBV-GN.
  • To determine if IFI16 senses HBV and influences the immune response in the context of HBV-GN.

Main Methods:

  • Immunohistochemistry (IHC) was used to assess IFI16, Caspase-1, and IL-1β expression in 75 kidney tissues (50 HBV-GN, 25 CGN).
  • In vitro studies utilized primary human glomerular mesangial (HGM) cells and HEK-293 T cells, co-transfected with HBV DNA and manipulated IFI16 expression (overexpression or silencing).
  • Quantitative Real-time PCR and western blotting analyzed gene and protein expression levels.

Main Results:

  • IFI16 expression was significantly higher in HBV-GN (80.0%) compared to CGN (24.0%) and correlated positively with HBV DNA, Caspase-1, and IL-1β.
  • Overexpression of IFI16 increased Caspase-1 and IL-1β in HBV-infected HGM and HEK-293 T cells.
  • IFI16 knockdown via siRNA downregulated Caspase-1 and IL-1β expression in both cell lines.

Conclusions:

  • Elevated IFI16 during HBV infection or replication may exacerbate renal damage through inflammation.
  • IFI16 represents a potential therapeutic target for HBV-GN.
  • This study opens new avenues for understanding the pathogenesis of HBV-GN.
Keywords:
Caspase-1HBV-DNAHBV-GNIFI16IL-1β

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