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Fig. 4 | Journal of Animal Science and Biotechnology

Fig. 4

From: Role of omega-3 polyunsaturated fatty acids, citrus pectin, and milk-derived exosomes on intestinal barrier integrity and immunity in animals

Fig. 4

Model summarizing the immunomodulatory and antimicrobial mechanisms of citrus pectin in the intestinal epithelium. (A) Pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) activate the nuclear factor-κB (NF-κB)-mediated pro-inflammatory response and damages the epithelial integrity as described in Fig. 3. (Black solid lines). Dietary citrus pectin (CPn) blocks the cell surface pattern-recognizing receptors (PRRs) and prevents the PAMPs or DAMPs from activating NF-κB (Red solid lines). (B) During infection or injury, extracellular Galectin-3 (Gal-3) acts as ligands to cell-surface PRRs and activates NF-κB-mediated pro-inflammatory response (Black solid lines). CPn can modify the cell-surface PRRs and prevent the Gal-3 from binding (Red solid lines). Alternatively, cells secrete intracellular Gal-3 that acts as PRRs to pathogens or endotoxins and recruits immune cells enabling opsonization (Black dotted lines). CPn can directly bind the intracellular Gal-3 and block its opsonin function (Red dotted lines). (C) CPn binds with mucin glycoproteins and forms gel-matrix that selectively support the adhesion of probiotics and gut commensals, while repel the pathogens (Red solid lines). Alternatively, CPn directly interacts with the pathogen and inhibits its growth or indirectly give rise to short-chain fatty acids (SCFAs) that protects barrier health (Red dotted lines). Abbreviations: ROS, Reactive oxygen species. For references, see text. Figure created using BioRender.com

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