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http://purl.uniprot.org/citations/35459254http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Aims and background

IFI16 plays an important role in innate immunity against invasive microbial infection by sensing double-stranded DNA viruses due to caspase-1-dependent inflammasome activation and subsequent maturation and secretion of IL-1β. However, the role of IFI16 in regulating the immune response to viruses in Hepatitis B Virus-Associated Glomerulonephritis (HBV-GN), especially in sensing hepatitis B virus (HBV), has not been determined. In this study, we investigated the inflammatory role of IFI16 in HBV-GN.

Methods

A total 75 kidney tissue including 50 HBV-GN and 25 chronic glomerulonephritis (CCN) were collected to determine the expression of IFI16, Caspase-1 and IL-1β using immunohistochemistry (IHC), then the correlation between them was analyzed. In vitro, the primary human glomerular mesangial (HGM) cells and HEK-293 T cell lines were used in this study. The cell lines were both co-transfected with HBVDNA and overexpression or silencing IFI16. Quantitative Real-time PCR and western blotting were used to determine the expression of IFI16, Caspase-1 and IL-1β.

Results

IFI16 expression in HBV-GN biopsies (80.0%) was significantly higher than in CGN (24.0%) and positively correlated with HBVDNA,caspase-1 and IL-1β expression in HBV-GN. Meanwhile, over expression of IFI16 increased caspase-1 and IL-1β expression in HBV-infected HGM and HEK-293 T cell lines, knockdown of IFI16 mRNA by siRNA resulted in downregulation of the caspase-1 and IL-1β expression in both cell lines.

Conclusions

The elevation of IFI16 during HBV infection or replication may contribute to renal damage due to inflammation, thus providing a putative therapeutic target and a new avenue for researching the pathogenesis of HBV-GN."xsd:string
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http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/author"Guo Y."xsd:string
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/author"Li C."xsd:string
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/author"Liu X."xsd:string
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http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/author"Zhao X."xsd:string
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/author"Xie S."xsd:string
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/author"Du W."xsd:string
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/name"Diagn Pathol"xsd:string
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http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/title"IFI16 induces inflammation in hepatitis B virus-associated glomerulonephritis by regulating the Caspase-1/ IL-1 ss pathway."xsd:string
http://purl.uniprot.org/citations/35459254http://purl.uniprot.org/core/volume"17"xsd:string
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