Leukocyte emigration in the early stages of laminitis.
Abstract: The mechanisms that initiate the pathophysiologic changes in the digital laminae in equine laminitis are poorly understood. Due to the fact that (1) the horse at risk of laminitis has many similarities clinically to the human sepsis patient and (2) our recent finding of marked laminar proinflammatory cytokine expression at the developmental time point of the black walnut extract (BWE) model of laminitis, we tested the possibility that, similar to organ damage in human sepsis, leukocyte emigration is an early event in laminitis. Using immunoperoxidase methods with an anti-equine CD13 monoclonal antibody that recognizes neutrophils and monocytes, we discovered that, whereas the dermal microvasculature of the skin commonly has a marginal pool of leukocytes, the normal laminar dermal microvasculature has minimal to no perivascular leukocytes. However, increases in leukocyte numbers occurred around the dermal vasculature of both the laminae and the skin in the majority of BWE-treated horses in the developmental stage and at the onset of clinical signs of lameness in the BWE model. These findings indicate that, similar to organ failure in human sepsis, leukocyte emigration is likely to play a significant role in initiating numerous pathophysiologic mechanisms that lead to the development of laminitis.
Publication Date: 2005-09-19 PubMed ID: 16169600DOI: 10.1016/j.vetimm.2005.08.017Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
This research investigates the factors that cause early changes in equine laminitis, a disease in horses. The study found that an increase in leukocytes, or white blood cells, around the dermal vasculature—which is similar to organ damage in human sepsis—may be a significant trigger for laminitis.
Overarching Aim of the Research:
- The ultimate goal of the study was to shed light on the unclear mechanisms that instigate the pathophysiologic alterations in the digital laminae, an important area related to laminitis in horses. The study drew parallels with the human sepsis patient to explore and better understand the early onset of equine laminitis.
Methodology of the Study:
- The researchers used immunoperoxidase methods with an anti-equine CD13 monoclonal antibody. This particular antibody recognizes and binds to neutrophils and monocytes, two types of white blood cells. These white blood cells were under scrutiny due to their parallels in human sepsis organ damage.
- The primary model of laminitis for the study was the black walnut extract (BWE) model. This model was chosen due to its demonstrated ability to induce noticeable laminar proinflammatory cytokine expression at the developmental stage.
Research Findings:
- The researchers observed that a marginal pool of leukocytes is commonly present in the dermal microvasculature of the skin. However, such leukocyte presence was found to be minimal or completely absent in the normal laminar dermal microvasculature.
- Key findings of the research included increases in leukocyte numbers around the dermal vasculature in both the laminae and the skin. This increase was observed predominantly in BWE-treated horses, more significantly in the developmental stage and the onset of clinical signs of lameness—a characteristic manifestation of laminitis—with the use of the BWE model.
Conclusions and Implications:
- Based on their findings, the researchers concluded that leukocyte emigration, much like in organ failure in human sepsis, appears to significantly contribute to triggering the pathophysiologic mechanisms that eventually lead to laminitis in horses.
- This study could open the doors for further research and potential therapeutic targets, as understanding the early stages of disease onset is critical for effective prevention and treatment strategies.
Cite This Article
APA
Black SJ, Lunn DP, Yin C, Hwang M, Lenz SD, Belknap JK.
(2005).
Leukocyte emigration in the early stages of laminitis.
Vet Immunol Immunopathol, 109(1-2), 161-166.
https://doi.org/10.1016/j.vetimm.2005.08.017 Publication
Researcher Affiliations
- Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01054, USA.
MeSH Terms
- Animals
- CD13 Antigens / immunology
- Cell Movement / immunology
- Disease Models, Animal
- Foot Diseases / immunology
- Foot Diseases / veterinary
- Horse Diseases / immunology
- Horses
- Immunohistochemistry / veterinary
- Leukocyte Count / veterinary
- Leukocytes, Mononuclear / immunology
- Skin Diseases / immunology
- Skin Diseases / veterinary
Citations
This article has been cited 10 times.- Storms N, Medina Torres C, Franck T, Sole Guitart A, de la Rebière G, Serteyn D. Presence of Myeloperoxidase in Lamellar Tissue of Horses Induced by an Euglycemic Hyperinsulinemic Clamp. Front Vet Sci 2022;9:846835.
- Ding J, Li S, Jiang L, Li Y, Zhang X, Song Q, Hayat MA, Zhang JT, Wang H. Laminar Inflammation Responses in the Oligofructose Overload Induced Model of Bovine Laminitis. Front Vet Sci 2020;7:351.
- Dern K, van Eps A, Wittum T, Watts M, Pollitt C, Belknap J. Effect of Continuous Digital Hypothermia on Lamellar Inflammatory Signaling When Applied at a Clinically-Relevant Timepoint in the Oligofructose Laminitis Model. J Vet Intern Med 2018 Jan;32(1):450-458.
- Dern K, Watts M, Werle B, van Eps A, Pollitt C, Belknap J. Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model. J Vet Intern Med 2017 Mar;31(2):575-581.
- Menzies-Gow NJ, Wray H, Bailey SR, Harris PA, Elliott J. The effect of tumour necrosis factor-α and insulin on equine digital blood vessel function in vitro. Inflamm Res 2014 Aug;63(8):637-47.
- Brooks AC, Menzies-Gow N, Bailey SR, Cunningham FM, Elliott J. Endotoxin-induced HIF-1alpha stabilisation in equine endothelial cells: synergistic action with hypoxia. Inflamm Res 2010 Sep;59(9):689-98.
- Johnson PJ, Wiedmeyer CE, Messer NT, Ganjam VK. Medical implications of obesity in horses--lessons for human obesity. J Diabetes Sci Technol 2009 Jan;3(1):163-74.
- Coyne MJ, Cousin H, Loftus JP, Johnson PJ, Belknap JK, Gradil CM, Black SJ, Alfandari D. Cloning and expression of ADAM-related metalloproteases in equine laminitis. Vet Immunol Immunopathol 2009 Jun 15;129(3-4):231-41.
- Faleiros RR, Macoris DG, Alves GE, Souza DG, Teixeira MM, Moore RM. Local and remote lesions in horses subjected to small colon distension and decompression. Can J Vet Res 2008 Jan;72(1):68-76.
- Zamith Cunha R, Gobbo F, Morini M, Salamanca G, Zanoni A, Bernardini C, Gramenzi A, Chiocchetti R. Cannabinoid and cannabinoid related receptors in fibroblasts, inflammatory and endothelial cells of the equine hoof with and without laminitis: novel pharmacological target. Front Vet Sci 2025;12:1723160.
Use Nutrition Calculator
Check if your horse's diet meets their nutrition requirements with our easy-to-use tool Check your horse's diet with our easy-to-use tool
Talk to a Nutritionist
Discuss your horse's feeding plan with our experts over a free phone consultation Discuss your horse's diet over a phone consultation
Submit Diet Evaluation
Get a customized feeding plan for your horse formulated by our equine nutritionists Get a custom feeding plan formulated by our nutritionists
