CRISPR screen links MYD88–IRAK4 signaling to fungal-toxin damage in pig intestinal cells
Published in Biology, Immunology, Journals, Tools, Toxicity.
Published October 30, 2026.
A Communications Biology study published October 28 uses a genome-wide CRISPR knockout screen to investigate how deoxynivalenol, a fungal toxin, damages pig intestinal epithelial cells.
The screen identified MYD88 and IRAK4 as leading contributors to susceptibility in the cultured-cell system. Exposure activated inflammatory signaling while reducing several antioxidant defenses and increasing reactive oxygen species and oxidized proteins.
Removing either gene improved cell survival during toxin exposure, reduced inflammatory responses and partly restored antioxidant protein levels. These experiments link inflammatory signaling with oxidative damage in this specific model.
The findings identify potential targets for further research into livestock toxin injury. They do not establish a treatment for exposed animals or humans, and gene knockout in cultured cells is not equivalent to a safe drug intervention. Studies in whole organisms would be needed to evaluate broader effects, including the consequences of altering immune-defense pathways.
Source: Yang et al., Communications Biology. Published October 28, 2026. DOI: 10.1038/s42003-026-11205-9.