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Abstract

Intestinal barrier function depends on epithelial adhesion, which restricts permeability and microbial invasion from the internal environment. Impairment of barrier integrity and gut function is closely linked to pro-inflammatory changes. Inflammation is often the primary factor that provokes gut function disorders. The anti-inflammatory potential of postbiotics has been reported in recent years. Muramyl peptides (MPs) are small signaling molecules that stimulate intracellular pathogen receptors and can regulate cell responses. However, the molecular mechanisms of MPs' effects on intestinal cells remain unknown. The study of MPs treatment on lipopolysaccharide (LPS)-challenged Caco-2 intestinal cells aimed to investigate the postbiotic effects on intestinal barrier integrity, autophagy, and inflammation. An in vitro inflammation model was constructed using Caco-2 cells exposed to 10-100 µg/mL of LPS. The results showed a dose-dependent decrease in cell viability and E-cadherin content. Conversely, TNF-α content was increased, confirming proinflammatory disturbances. No significant differences were detected in cells exposed to 5-50 µg/mL doses of MPs. However, treatment with 50 µg/mL MPs ameliorated TNF-α production in LPS-exposed cells. The application of 20 and 50 µg/mL MPs exhibited a cytoprotective effect on cell viability in a dose-dependent manner. Furthermore, the 50 µg/mL dose of MPs ameliorated the reduction of E-cadherin content induced by LPS exposure. MPs treatment did not modulate the conversion of the autophagosome marker LC3-I into LC3-II but upregulated its content in LPS-challenged cells. These results demonstrate that MPs may be a promising tool to restore inflammatory balance and maintain intestinal barrier function.

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Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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