On failing in pregnancy.

Intestinal inflammation represents a critical challenge in both human and animal health, as disruption of epithelial barrier integrity directly affects nutrient absorption, immune homeostasis, and metabolic performance (–). In livestock and companion animal production systems, even subclinical intestinal inflammation can impair feed conversion efficiency, reduce growth rates, alter microbial composition, and increase susceptibility to enteric infections (, ). At the molecular level, intestinal inflammation is frequently driven by microbe-derived pathogen-associated molecular patterns (PAMPs), particularly lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria and a microbiota-produced PAMP (–). Recognition of LPS by the Toll-like receptor 4 (TLR4)/MD-2/CD14 signaling complex activates downstream NF-κB-dependent inflammatory pathways, resulting in the production of pro-inflammatory cytokines, chemokines, and mediators that contribute to epithelial dysfunction and increased intestinal permeability (, ). Persistent activation of these inflammatory cascades promotes disruption of tight junction architecture, facilitates translocation of luminal microbial products, and amplifies local immune activation, ultimately compromising intestinal barrier homeostasis (). Consequently, strategies capable of reducing LPS-induced inflammatory signaling or preserving epithelial barrier integrity have attracted increasing interest as supportive approaches for improving intestinal health and resilience in both veterinary and biomedical settings (). LPS activates Toll-like receptor 4 (TLR4) on epithelial and immune cells, triggering downstream signaling cascades involving MyD88- and TRIF-dependent pathways, culminating in activation of the nuclear factor kappa B (NF-κB) transcription factor (–). This signaling axis drives the expression of pro-inflammatory cytokines, including INF-y, TNF-α, IL-6, IL-8, and inducible nitric oxide synthase (iNOS), perpetuating mucosal immune activation and contributing to chronic low-grade inflammation (, ). Persistent activation of this pathway compromises epithelial barrier function and exacerbates metabolic inefficiencies in production animals. Given the global reduction in antibiotic use in animal agriculture and the increasing demand for sustainable feed solutions, there is a pressing need for non-pharmacological strategies capable of modulating endotoxin-driven inflammation at the intestinal interface (, ). Rather than directly suppressing immune signaling, an alternative approach involves reducing the luminal bioavailability of inflammatory triggers such as LPS before they engage host receptors ().