ArticlePoultry science2026
Ligilactobacillus salivarius 8-2 attenuates intestinal mucosal injury in chicks via the mitochondrial fision-glycometabolism reprogramming axis.
Article in Poultry science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The intestinal mucosa is crucial for nutrient absorption and barrier function. In this study, a newly identified strain of Ligilactobacillus salivarius (L. sa. 8-2) exhibited a mucosal protective effect in chick intestinal injury models. However, the underlying mechanisms need to be clarified. In vivo, chicks were pre-fed with L. sa. 8-2 supernatant or its precipitate and then challenged with lipopolysaccharide (LPS) or Salmonella Typhimurium (STm). The results showed that L. sa. 8-2 and its supernatant significantly reduced intestinal epithelial apoptosis, increased goblet cell density and Muc2 mRNA abundance, and upregulated Claudin1 protein levels. Specifically, compared with the LPS-challenged group, L. sa. 8-2 supernatant accelerated epithelial renewal, as shown by elevated protein levels of proliferating cell nuclear antigen (PCNA) and increased mRNA abundance of cell cycle regulators Ccnd1 and Cdk2. Moreover, the L. sa. 8-2 supernatant markedly increased protein levels of both the active intestinal stem cell (aISC) marker LGR5 and the reserve ISC (rISC) marker HOPX in the intestinal crypt. In vitro, the enteroids were pre-treated with L. sa. 8-2 supernatant and then challenged with LPS. It was shown that the L. sa. 8-2 supernatant elevated the protein levels of LGR5 and HOPX compared with the injured group. Moreover, co-staining of LGR5 and HOPX revealed that more HOPX
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