Feeding the inflammasome to damage the liver
In-person only
Liver injury and inflammation are the major factors triggering the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Mechanisms for inflammation inhibition must exist to allow tissue resolution. Here, we use a novel knock-in mouse model to suppress Caspase-1 (CASP1) deactivation and thus prolong CASP1 activity. We fed mice a methionine-choline-deficient diet (MCD), to induce key features of MASLD, including inflammation, liver steatosis, and liver damage. Indeed, each of these features was elevated in Casp1.CDL mice compared to WT animals. Modelling a “lifestyle intervention”, we fed mice an MCD diet to induce MASLD and then switched to a healthier control diet, which resulted in liver recovery in WT mice, while Casp1.CDL mice had a delay in disease resolution. Our research findings address the important question of whether in vivo mechanisms for signal inhibition, such as self-limiting CASP1 activation, prevent disease progression in MASLD.
Date:
1 July 2024, 12:00 (Monday, 11th week, Trinity 2024)
Venue:
Kennedy Institute of Rheumatology, Headington OX3 7FY
Venue Details:
Kennedy Lecture Theatre
Speaker:
Dr Sabrina Sofia Burgener (University of Queensland)
Organising department:
Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS)
Organiser:
Doris Chan (Kennedy Institute of Rheumatology)
Organiser contact email address:
doris.chan@kennedy.ox.ac.uk
Host:
Dr Jelena Bezbradica (The Kennedy Institute of Rheumatology)
Part of:
Kennedy Institute Seminars
Booking required?:
Not required
Audience:
Members of the University only
Editor:
Doris Chan
