A study published in Nature Microbiology on June 6, led by Prof. Xu Daichao from the Shanghai Institute of Organic Chemistry, has identified a molecular link between glucose sensing and non-classical pyroptosis, a form of inflammatory cell death.

Pyroptosis and nutritional status are crucial in defending against pathogens, with glucose levels playing a key role in this process.

During bacterial infection, glucose levels in host cells fluctuate, potentially as part of the immune response.

The study found that Yersinia infection increases glycolysis in immune cells, decreasing glucose levels and overactivating AMPK, an energy-sensing enzyme.

This overactivation inhibits the RIPK1-caspase-8-GSDMD pathway, preventing pyroptosis and worsening the infection.

Experiments showed that overactivating AMPK worsened infection, while inhibiting AMPK or supplementing glucose improved resistance to Yersinia.

The findings highlight the importance of maintaining glucose homeostasis in treating infections, as it affects AMPK activation and immune response.