Mycotoxins are toxic secondary metabolites produced by filamentous fungi that contaminate agricultural commodities, posing risks to food safety, animal productivity, and human health. The gastrointestinal tract is the first and most critical site of exposure, where the intestinal epithelium functions as both a physical and immunological barrier against luminal toxins and pathogens. While extensive research has demonstrated that mycotoxins disrupt epithelial integrity through tight junction impairment, oxidative stress, apoptosis, and inflammation, their effects on the intestinal stem cell (ISC) compartment and epithelial regeneration remain insufficiently understood. This review integrates recent findings from in vivo, cell culture, and advanced 3D intestinal organoid and gut-on-chip models to elucidate how mycotoxins such as deoxynivalenol and zearalenone impair ISC proliferation, alter Wnt/Notch signaling, and compromise mucosal repair. We also discuss dose relevance, species differences, and the modulatory roles of the microbiome and short-chain fatty acids, as well as emerging evidence of additive or synergistic toxicity under co-exposure conditions. By bridging well-established mechanisms of barrier disruption with the emerging concept of ISC-driven regenerative failure, this review identifies a critical knowledge gap in mycotoxin toxicology and highlights the need for integrative models that link epithelial damage to impaired regeneration. Collectively, these insights advance understanding of mycotoxin-induced intestinal dysfunction and provide a foundation for developing nutritional, microbial, and pharmacological strategies to preserve gut integrity and repair.

Rotavirus (RV) remains a leading cause of severe gastroenteritis in infants and young animals worldwide, contributing to significant morbidity and mortality despite the availability of vaccines. The gastrointestinal tract’s health, shaped by complex interactions between nutrition, the gut microbiota, and the host immune system, plays a crucial role in RV pathogenesis and outcomes. Emerging evidence suggests that dietary components not only influence the composition and function of the gut microbiota but also modulate immune responses essential for protection against RV. This review integrates findings from human and animal models to elucidate the interplay between nutrition, microbiota, and immunity in the context of RV infection. We aim to shed light on the mechanisms by which dietary factors and microbial communities influence RV susceptibility and severity, and how this knowledge could guide the development of more effective preventive and therapeutic strategies.

The purpose of this study was to examine the effect of daidzein on the proliferation of porcine mammary epithelial cells (PMECs) and elucidate the underlying molecular mechanisms. PMECs were treated with varying daidzein or rapamycin levels, and then cell proliferation and mTOR pathway protein expression were detected. When the concentration of daidzein added was in the range of 0–80 μM, cell proliferation was significantly promoted (p < 0.05). These results were in agreement with those obtained using the 5-ethynyl-2′-deoxyuridine (EdU) assay. Daidzein administration at 20 and 40 μM concentrations triggered significant activation of the mTOR signaling cascade and enhanced expression of downstream cell-cycle-regulatory proteins (cyclin D1) (p < 0.05). Moreover, exposure to 40 μM daidzein attenuated apoptotic signaling, as evidenced by reduced levels of Bax protein and cleaved caspase-3 (p < 0.05). These effects were reversed when rapamycin was used to inhibit the mTOR pathway. In conclusion, our findings suggest that daidzein activates PMEC proliferation via the mTOR pathway. The present work not only characterizes new functional properties of daidzein but also establishes mechanistic evidence supporting its role in augmenting sow lactation efficiency.