The cytosolic LPS-sensing pathway mediated by caspase-4/5/11 is regarded as the final line of host defense. When this defensive line is triggered, the host immune system may respond in extreme ways, including cytokine storm and inflammatory cell death, leading to sepsis. Galectin-3 recognizes cytosolic LPSs from various bacteria and amplifies LPS-induced caspase-4/11 oligomerization and activation, causing a more intense inflammatory response. By intracellularly recognizing LPS glycan moieties, galectin-3 may act as a critical regulator of LPS-mediated sepsis. The results were published in PNAS on July 27, 2021.

Article Link: https://doi.org/10.1073/pnas.2026246118

A critical molecule for regulating inflammatory cell death through intracellular binding to microbial glycans