Laminar Chemokine MRNA Concentrations in Horses With Carbohydrate Overload-Induced Laminitis

Article Outline

• Take Home Message
• Introduction
• Material and Methods
• Results
• Discussion
• Clinical Relevance and Conclusion
• Copyright

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Take Home Message 

Chemokines may be considered as possible therapeutic targets in equine laminitis.

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Introduction 

We have described increased gene expression of the key chemokines interleukin-8 (IL-8) and CXCL1 in horses with Black Walnut extract (BWE, both chemokines) and fructose-induced (IL-8) laminitis. The purpose was to evaluate laminar chemokine gene expression in horses with classical carbohydrate overload (CHO)-induced laminitis.

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Material and Methods 

Frozen laminar samples were obtained 24 h following water administration (CON, n=7), at onset of fever (10-20 hours, DTP group, n=6), and at the onset of lameness (20-46 hours, LAM group, n=6) following CHO administration. Quantitative real time PCR was performed in all samples in order to determine mRNA concentrations of the following chemokines: CXCL1, CXCL6, IL-8 (CXCL8) and monocyte chemotactic protein-1 (MCP1) and MCP2. Data was expressed as fold change compared with control mean and subjected to ANOVA followed by Student-Newman-Keuls (P < 0.05).

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Results 

Whereas some laminar chemokine mRNA concentrations were increased at DTP all peaked at the onset of lameness (LAM group). These (recorded as fold increases at LAM vs. control, listed in descending order of magnitude of peak increase) include: IL-8 (91-fold), CXCL6 (72-fold) and MCP1 (24-fold) followed by CXCL1 (8.7-fold) and MCP2 (3.4-fold at LAM). MCP1 and MCP2 were only increased at the onset of lameness.

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Discussion 

Aligned with our previous studies, CXCL1, CXCL6 and IL-8 increases preceded leukocyte laminar accumulation. Additionally, MCP1 and MCP2 expressions corroborate previous reports of monocyte/macrophage laminar accumulation.

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Clinical Relevance and Conclusion 

Increased laminar chemokine gene expression consistently precedes leukocyte accumulation and onset of lameness in BWE and CHO laminitis models.