Calprotectin in myeloid and epithelial cells of laminae from horses with black walnut extract-induced laminitis.
Authors: Faleiros, Nuovo, Belknap
Journal: Journal of veterinary internal medicine
Summary
Laminar inflammation precedes structural failure in laminitis, yet the molecular mechanisms driving early epithelial dysfunction remain incompletely understood. Faleiros and colleagues investigated calprotectin (CP), a damage-associated molecular pattern protein implicated in inflammatory skin conditions, within laminar tissue from 20 horses following black walnut extract administration or control treatment, using immunohistochemistry to localise CP expression and quantify inflammatory cell infiltration at 1.5, 3, and 12 hours post-treatment. Significantly elevated calprotectin signal appeared in the laminar epidermis at the 3-hour timepoint (P = 0.02), coinciding with marked increases in perivascular polymorphonuclear neutrophils and mononuclear cells compared to controls (P = 0.003), with CP-positive leukocytes clustering particularly near the epidermal basement membrane. The authors' key observation—that CP expression follows rather than precedes leukocyte extravasation—suggests that neutrophil migration into laminar tissue may trigger epithelial stress and initiate the inflammatory cascade culminating in lamellar failure. For practitioners, these findings support the concept that early laminitis involves leukocyte-mediated epithelial injury driven by damage-associated molecular patterns, potentially identifying future therapeutic targets aimed at limiting neutrophil infiltration or downstream inflammatory signalling before irreversible structural damage occurs.
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Practical Takeaways
- •Calprotectin may serve as a biomarker for early-stage laminitis development and could aid in diagnostic protocols for detecting laminar inflammation before clinical signs appear
- •Understanding that PMN infiltration precedes epithelial calprotectin expression supports the importance of early anti-inflammatory interventions targeting leukocyte recruitment in laminitis cases
- •This molecular pathway identification opens potential therapeutic targets for preventing laminar failure by interrupting leukocyte-mediated epithelial stress mechanisms
Key Findings
- •Laminar epidermal calprotectin signal was significantly increased (P=0.02) at the laminitis time point compared with control groups
- •Marked increases in leukocyte numbers were detected in BWE-treated groups (P=0.003) compared with rare leukocytes in control laminae
- •The majority of calprotectin-positive leukocytes were perivascular polymorphonuclear neutrophils at all developmental time points
- •Calprotectin expression in laminar epidermis occurs after leukocyte extravasation, suggesting leukocyte emigration is an initiating factor in laminar epithelial inflammation