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Lactobacillus rhamnosus GG is a human-derived probiotic known to support intestinal health and immune regulation in mammals. However, evidence demonstrates that it causes intestinal damage in zebrafish. Specifically, the SpaC pilin component of the bacterium triggers cell pyroptosis, an inflammatory form of cell death, and disrupts the gut microbiome. In zebrafish, dietary SpaC is recognised by the TLR4ba receptor, activating the Caspase-3-GSDMEa pathway. This reaction induces pyroptosis in the intestinal lining and increases the presence of lipopolysaccharide-producing bacteria, which in turn triggers a secondary Gaspy2-GSDMEb cell death pathway. Because this harmful mechanism relies on species-specific receptor recognition, the findings demonstrate that probiotics beneficial to one host can cause injury in another, underscoring safety considerations when administering probiotics across different animal species.
Probiotics are widely consumed to improve gut health, but their safety is often assumed to transfer across different organisms. Demonstrating that a well-established mammalian probiotic causes severe gut inflammation and microbial disruption in fish reveals that beneficial effects depend heavily on the host. This highlights the importance of species-specific safety assessments before introducing microbes into new environments or animal diets.
This early-stage research informs feed developers, aquaculture health companies, and regulatory bodies evaluating microbial additives. It demonstrates that mammalian-derived probiotics cannot simply be repurposed for aquatic species without risk of inducing intestinal damage. While the abstract establishes a clear safety parameter to consider during product development, it offers mechanistic laboratory findings rather than a validated commercial formulation or testing tool, placing practical commercial use at an early exploratory stage.
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<i>Lactobacillus rhamnosus</i> GG (LGG), the well-characterized human-derived probiotic strain, possesses excellent properties in the maintenance of intestinal homeostasis, immunoregulation and defense against gastrointestinal pathogens in mammals. Here, we demonstrate that the SpaC pilin of LGG causes intestinal epithelium injury by inducing cell pyroptosis and gut microbial dysbiosis in zebrafish. Dietary SpaC activates Caspase-3-GSDMEa pathways in the intestinal epithelium, promotes intestinal pyroptosis and increases lipopolysaccharide (LPS)-producing gut microbes in zebrafish. The increased LPS subsequently activates Gaspy2-GSDMEb pyroptosis pathway. Further analysis reveals the Caspase-3-GSDMEa pyroptosis is initiated by the species-specific recognition of SpaC by TLR4ba, which accounts for the species-specificity of the SpaC-inducing intestinal pyroptosis in zebrafish. The observed pyroptosis-driven gut injury and microbial dysbiosis by LGG in zebrafish suggest that host-specific beneficial/harmful mechanisms are critical safety issues when applying probiotics derived from other host species and need more attention.
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DOI: 10.1002/imt2.181
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