Postbiotics Suppress Infection via Modulating Bacterial Pathogenicity, Autophagy and Inflammasome in Mice.

Our study aimed to explore the effects of postbiotics on protecting against infection in mice and clarify the underlying mechanisms. Eighty 5-week-old C57BL/6 mice were gavaged daily with (LP)-derived postbiotics (heat-killed bacteria, LPB; culture supernatant, LPC) or the active bacteria (LPB), and gavaged with Typhimurium (ST). The Turbidimetry test and agar diffusion assay indicated that LPC directly inhibited growth. Real-time PCR and biofilm inhibition assay showed that LPC had a strong ability in suppressing pathogenicity by reducing virulence genes (, , , , , , and 2), pili genes (, , , ), flagellum genes (, , ) and biofilm formation. LP postbiotics were more effective than LP on attenuating ST-induced intestinal damage in mice, as indicated by increasing villus/crypt ratio and increasing the expression levels of tight junction proteins (Occludin and Claudin-1). Elisa assay showed that LP postbiotics significantly reduced ST-induced inflammation by regulating the levels of inflammatory cytokines (the increased IL-4 and IL-10 and the decreased TNF-α) in serum and ileum ( < 0.05). Furthermore, LP postbiotics inhibited the activation of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome by decreasing the protein expression of NLRP3 and Caspase-1, and the gene expression of -, and -. Meanwhile, both LPC and LPB observably activated autophagy under ST infection, as indicated by the up-regulated expression of LC3 and Beclin1 and the downregulated p62 level ( < 0.05). Finally, we found that LP postbiotics could trigger an AMP-activated protein kinase (AMPK) signaling pathway to induce autophagy. In summary, -derived postbiotics alleviated infection via modulating bacterial pathogenicity, autophagy and NLRP3 inflammasome in mice. Our results confirmed the effectiveness of postbiotics agents in the control of infection.