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In IBD, the expression levels of tight junction proteins such as ZO-1 and Occludin, is generally suppressed, leading to increased intestinal permeability, enhanced pathogen infiltration, and exacerbated inflammatory responses (Dong et al., 2022)

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NCR has been described to respond to glutamine and glutamate deficiencies through the activation of Gln3 or Gat1 respectively, while ammonium is considered a distinct signal for NCR that acts independently of the glutamine and glutamate levels [34]