Decoding Equine Colitis: Emerging Insights into the Pathophysiology and Disease Mechanisms

Presentation Description / Summary: In acute equine colitis, the endothelial glycocalyx (EG) integrity, bidirectional gut permeability, the enteroinsular axis (EIA, insulin and incretins), mineral homeostasis, vitamin D concentrations, and bone remodelling play crucial roles in disease pathophysiology and outcome. The EG is a protective layer on the vascular endothelium that maintains vascular homeostasis. Damage to this structure during colitis can increase vascular permeability, inflammation, and edema. Gut permeability is also significant; in equine colitis, increased concentrations of certain markers indicate that the barrier function can be compromised, allowing the leak of water, electrolytes, and proteins into the lumen but also translocation of harmful substances into the bloodstream, exacerbating systemic inflammation. Insulin and glucagon-like peptide-1 (GLP-1) are involved in energy homeostasis. In addition, GLP-1 has anti-inflammatory and cytoprotective effects. GLP-1 alterations in colitis can potentially impair gut motility, increase intestinal inflammation, and hinder mucosal healing, exacerbating disease progression. Vitamin D is essential for calcium and phosphorus homeostasis, epithelial integrity and immune regulation. Vitamin D deficiency during colitis, in addition to reduced calcium and phosphorus absorption, could exacerbate the inflammatory response, leading to secondary metabolic bone disease and bacterial invasion. Bone remodelling, a process dependent on the balance between osteoclast and osteoblast activity, is also affected. Inflammatory cytokines and altered calcium homeostasis during colitis can disrupt normal bone remodelling, leading to excessive bone loss. The objective of this lecture is to present recent findings on EG integrity, gut permeability, the EIA, mineral homeostasis, vitamin D and associated regulatory factors, and bone remodelling of horses with colitis.