Laminar inflammatory events in lean and obese ponies subjected to high carbohydrate feeding: Implications for pasture-associated laminitis.
Authors: Burns T A, Watts M R, Weber P S, McCutcheon L J, Geor R J, Belknap J K
Journal: Equine veterinary journal
Summary
# Editorial Summary Burns and colleagues investigated whether moderate, sustained dietary carbohydrate elevation triggers the same laminar inflammatory cascade implicated in acute carbohydrate overload laminitis, using 22 ponies stratified by body condition (lean or obese) and assigned to either a low-NSC control diet (~7% NSC) or a high-NSC challenge diet (~42% NSC) for seven days. Through immunohistochemistry and quantitative PCR analysis of laminar tissue, the researchers examined infiltration of inflammatory cells (CD163+ and MAC387+ populations) alongside expression of key pro-inflammatory mediators including interleukins, TNF-α, COX-2, adhesion molecules, and nitric oxide synthase. Despite the substantial dietary carbohydrate challenge, high NSC feeding produced no increase in laminar proinflammatory cytokine expression and no detectable leucocyte infiltration; only COX-2 expression increased in response to the high carbohydrate diet, regardless of body condition. These findings suggest that pasture-associated laminitis may operate through a mechanistically distinct pathway from the robust systemic inflammation characteristic of sepsis-triggered laminitis, implying that pasture-related disease likely involves local metabolic or vascular changes rather than the acute inflammatory cell recruitment seen in other laminitis models—a distinction with significant implications for targeting therapeutic interventions toward the true pathophysiological drivers of grazing-related disease.
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Practical Takeaways
- •Acute pasture-associated laminitis may develop through different inflammatory mechanisms than sepsis-associated laminitis, potentially involving metabolic rather than classical inflammatory pathways
- •The absence of significant leucocyte infiltration and proinflammatory cytokine upregulation with high carbohydrate feeding suggests prevention strategies for pasture laminitis may need to focus on metabolic regulation rather than anti-inflammatory interventions alone
- •Both lean and obese ponies showed similar laminar responses to carbohydrate challenge, indicating body condition score alone does not predict inflammatory susceptibility in this experimental model
Key Findings
- •High carbohydrate feeding (42% NSC) for 7 days did not increase laminar proinflammatory cytokine expression (IL-1β, IL-6, TNF-α, IL-8, MCP-1, MCP-2) in either lean or obese ponies
- •Laminar COX-2 expression was increased by high carbohydrate feeding, indicating some inflammatory response at the molecular level
- •No laminar leucocyte infiltration (CD163+ or MAC387+ cells) was observed in response to high carbohydrate feeding
- •Marked laminar inflammation characteristic of sepsis-associated laminitis did not occur with moderate, prolonged carbohydrate challenge, suggesting different pathophysiological mechanisms between pasture-associated and sepsis-associated laminitis