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Overall, dysregulated cytokine signaling, particularly involving TGF-β and IL-33, along with NO-mediated oxidative stress, contribute significantly to the pathogenesis of IBD, highlighting potential therapeutic targets for intervention (221, 222) ( Figure 9 )
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Similarly, heat-stable bacteriocins, including nisin, can retain antimicrobial functionality after severe thermal exposure, supporting their integration into thermally processed food products 2
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