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There is a bidirectional link between the two phenomena: an increase in permeability promotes dysbacteriosis ( + (CD4 + ) T-cell expansion and interleukin 17A production that limits enteric pathogen invasion ( Salmonella typhimurium infection is more severe in transgenic mice with increased intestinal permeability, suggesting that barrier defects ultimately result in enhanced disease progression despite the activation of protective mucosal immunity ( Intestinal mucus is a critical component of the IEB since it forms a direct link between the host and the microbiota

625 RNAi-mediated screening revealed that ALOX5 is the primary factor required for ACSL4-independent ferroptosis induced by mutant huntingtin protein HTTQ94