Laminar inflammatory gene expression in the carbohydrate overload model of equine laminitis.
Authors: Leise B S, Faleiros R R, Watts M, Johnson P J, Black S J, Belknap J K
Journal: Equine veterinary journal
Summary
# Editorial Summary: Laminar Inflammatory Gene Expression in Carbohydrate Overload Laminitis Carbohydrate overload-induced laminitis more closely mirrors the sepsis-related cases seen clinically than traditional toxin models, making it a valuable research platform for understanding disease mechanisms. Leise and colleagues administered a massive starch bolus (17.6 g/kg bodyweight) via nasogastric tube to 16 horses, collecting laminar tissue samples either when fever developed (>38.9°C) or at the onset of Obel grade 1 lameness, then used quantitative PCR to measure inflammatory gene expression in comparison with control horses. Laminae from horses showing clinical lameness displayed significantly elevated messenger RNA concentrations for interleukin-1β, interleukin-6, interleukin-12p35, COX-2, E-selectin and ICAM-1, whereas earlier febrile stages and control animals did not. Critically, the inflammatory cascade in the carbohydrate overload model appears compressed temporally compared with black walnut extract models, with multiple laminar inflammatory events—endothelial activation, leucocyte emigration and cytokine expression—occurring simultaneously at or immediately before the onset of clinical lameness rather than during earlier developmental phases. These findings reinforce that inflammatory signalling is fundamental to laminitis pathophysiology across different disease models, with important implications for the timing and targeting of anti-inflammatory interventions in clinical cases.
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Practical Takeaways
- •The CHO model more closely resembles clinical sepsis-related laminitis than other experimental models, making findings more relevant to naturally occurring cases on farms
- •Significant laminar inflammation occurs at or very near the onset of visible lameness in carbohydrate overload scenarios, suggesting early intervention may be critical before substantial inflammatory cascade is established
- •Multiple inflammatory pathways are activated simultaneously in the CHO model (endothelial, leucocyte, and cytokine responses), indicating treatment strategies targeting single inflammatory mediators may be insufficient
Key Findings
- •Increased mRNA concentrations of IL-1β, IL-6, IL-12p35, COX-2, E-selectin and ICAM-1 were present in laminae at onset of Obel grade 1 lameness (P<0.05) but not at earlier developmental stages in the CHO model
- •The temporal pattern of inflammatory response in the CHO model differs from the BWE model, with most inflammatory events clustering at or near onset of lameness rather than peaking in earlier developmental stages
- •Local laminar phenomenon in CHO model may result in simultaneous endothelial activation, leucocyte emigration and proinflammatory cytokine expression
- •Inflammatory signalling is a consistent pathophysiological entity across different laminitis models despite differences in temporal expression patterns