Bif1 inhibits activation of inflammasome through autophagy regulatory mechanism.
Mol Med Rep
; 29(4)2024 04.
Article
en En
| MEDLINE
| ID: mdl-38456519
ABSTRACT
Inflammasome activation is a crucial mechanism in inflammatory responses. Baxinteracting factor 1 (Bif1) is required for the normal formation of autophagosomes, but its ability to exert an inflammatory regulatory effect remains unclear. The aim of the present study was to explore the role of Bif1 in inflammation, possibly mediated through autophagy regulation. Using a lipopolysaccharide (LPS)/adenosine triphosphate (ATP)induced inflammatory model in J774A.1 cells, the effect of Bif1 on inflammasome activation and the underlying mechanisms involving autophagy regulation were investigated. Elevated levels of NLR family pyrin domain containing protein 3 inflammasome and interleukin1ß (IL1ß) proteins were observed in J774A.1 cells after LPS/ATP induction. Furthermore, Bif1 and autophagy activity were significantly upregulated in inflammatory cells. Inhibition of autophagy resulted in inflammasome activation. Silencing Bif1 expression significantly upregulated IL1ß levels and inhibited autophagy activity, suggesting a potential antiinflammatory role of Bif1 mediated by autophagy. Additionally, inhibition of the nuclear factorκB (NFκB) signaling pathway downregulated Bif1 and inhibited autophagy activity, highlighting the importance of NFκB in the regulation of Bif1 and autophagy. In summary, the current study revealed that Bif1 is a critical antiinflammatory factor against inflammasome activation mediated by a mechanism of autophagy regulation, indicating its potential as a therapeutic target for inflammatory regulation.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Inflamasomas
/
Proteína con Dominio Pirina 3 de la Familia NLR
Idioma:
En
Revista:
Mol Med Rep
Año:
2024
Tipo del documento:
Article
Pais de publicación:
Grecia