
녹농균의 VgrG2b 단백질은 숙주 세포의 카스파제-11에 의해 절단되어 NLRP3 인플라마좀 활성화를 억제하는 C-말단 단편을 생성함으로써 숙주의 면역 반응을 회피하고 감염을 촉진한다.


coremsg

The T6SS of Pseudomonas aeruginosa plays an essential role in the establishment of chronic infections. Inflammatory cytokines mediated by inflammasomes are crucial for the body to resist bacterial infections. Here we found that during the infection of P. aeruginosa , non-canonical inflammasome was activated in macrophages, but the activation of downstream NLRP3 inflammasome was inhibited. The VgrG2b of P. aeruginosa is recognized and cleaved by caspase-11, generating a free C-terminal fragment. The VgrG2b C-terminus can bind to NLRP3, inhibiting the activation of the NLRP3 inflammasome by rejecting NEK7 binding to NLRP3. Administrating a specific peptide that inhibits the cleavage of VgrG2b by caspase-11 to mice can significantly improve their survival rate during infection. Our discovery elucidates a mechanism by which P. aeruginosa inhibits host immune response, providing a new approach for the future clinical treatment of P. aeruginosa infections.

### Competing Interest Statement

The authors have declared no competing interest.

A VgrG2b fragment cleaved by caspase-11/4 promotes Pseudomonas aeruginosa infection through suppressing the NLRP3 inflammasome

카스파제-11-4에-의해-절단된-vgrg2b-단편은-nlrp3-인플라마좀-억제를-통해-녹농균-감염을-촉진한다


카스파제-11/4에 의해 절단된 VgrG2b 단편은 NLRP3 인플라마좀 억제를 통해 녹농균 감염을 촉진한다
