Expression of inflammation-associated genes in circulating leukocytes collected from horses with gastrointestinal tract disease.
Abstract: To investigate whether expression of inflammation-associated genes in leukocytes from horses with gastrointestinal tract (GIT) diseases correlated with the type of disease and outcome. Methods: 10 healthy horses and 50 horses with GIT disease. Methods: A blood sample was collected from each healthy horse or horse with GIT disease (during admission to the hospital). Leukocytes were isolated, diluted to a standard concentration, and frozen until RNA extraction. Expression of 14 genes associated with inflammation was quantified by use of a real-time quantitative reverse transcription PCR assay. Results were grouped by GIT disease type and disease outcome for comparison. Results: Horses with GIT disease had colic of unknown etiology (n = 8 horses), GIT inflammation or strangulation (19), or nonstrangulating GIT obstruction (23). Among the 45 horses receiving treatment, 38 were discharged from the hospital, and 7 died or were euthanized. Compared with healthy horses, horses with colic of unknown etiology had similar gene expression. Significant differences in expression of the interleukin-8, leukocyte-selectin molecule, matrix metalloproteinase-9, platelet-selectin molecule, mitochondrial superoxide dismutase, Toll-like receptor 4, and tumor necrosis factor-A genes were detected between healthy horses and horses with GIT disease. Significant differences in expression of the interleukin-1 receptor antagonist, interleukin-8, leukocyte-selectin molecule, matrix metalloproteinase-9, platelet-selectin molecule, mitochondrial superoxide dismutase, Toll-like receptor 4, and tumor necrosis factor-A genes were detected among healthy horses and horses grouped by disease outcome. Conclusions: Inflammatory gene expression in leukocytes of horses with GIT disease appeared to be related to disease pathogenesis and prognosis.
Publication Date: 2010-08-03 PubMed ID: 20673091DOI: 10.2460/ajvr.71.8.915Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research article investigates the connection between the expression of certain inflammation-related genes in leukocytes (a type of white blood cell) and the type and outcome of gastrointestinal tract (GIT) diseases in horses. The study found that these gene expressions were indeed related to the cause and prognosis of these GIT diseases.
Methodology
- The study was conducted on a sample population of 10 healthy horses and 50 horses suffering from various GIT diseases.
- Blood was drawn from both the healthy and diseased horses upon their admission to the hospital.
- Leukocytes were then separated from the blood sample, made uniform in concentration and stored to extract RNA later.
- Real-time quantitative reverse transcription PCR assay was then used to quantify the expression of 14 inflammation associated genes.
- The results of gene expressions were then grouped by the type of GIT disease and the outcome of the disease for comparison purposes.
Results
- The diseases in the horse sample population consisted of colic of unknown cause (8 horses), GIT inflammation or strangulation (19 horses), and nonstrangulating GIT obstruction (23 horses).
- Out of the 45 horses that underwent treatment, 38 were discharged and 7 died or had to be put down.
- Compared to the healthy horse group, horses with colic exhibited similar gene expression patterns.
- Significant differences were found in the expression of genes like interleukin-8, leukocyte-selectin molecule, matrix metalloproteinase-9, platelet-selectin molecule, mitochondrial superoxide dismutase, Toll-like receptor 4, and tumor necrosis factor-A between healthy horses and the ones suffering from GIT diseases.
- Among healthy horses and groups divided by disease outcome, significant differences were detected in the expression of the interleukin-1 receptor antagonist, interleukin-8, leukocyte-selectin molecule, matrix metalloproteinase-9, platelet-selectin molecule, mitochondrial superoxide dismutase, Toll-like receptor 4, and tumor necrosis factor-A genes.
Conclusions
- Based on the observed gene expression patterns, the study concluded that inflammation related gene expression in horse leukocytes seemed to be associated with the cause and prognosis of GIT diseases.
Cite This Article
APA
Lopes MA, Salter CE, Vandenplas ML, Berghaus R, Hurley DJ, Moore JN.
(2010).
Expression of inflammation-associated genes in circulating leukocytes collected from horses with gastrointestinal tract disease.
Am J Vet Res, 71(8), 915-924.
https://doi.org/10.2460/ajvr.71.8.915 Publication
Researcher Affiliations
- Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA. maflopes@gmail.com
MeSH Terms
- Animals
- Colic / blood
- Colic / genetics
- Colic / physiopathology
- Colic / veterinary
- DNA / genetics
- DNA / isolation & purification
- Euthanasia
- Gastrointestinal Diseases / genetics
- Gastrointestinal Diseases / mortality
- Gastrointestinal Diseases / physiopathology
- Gastrointestinal Diseases / veterinary
- Horse Diseases / blood
- Horse Diseases / genetics
- Horse Diseases / mortality
- Horse Diseases / physiopathology
- Horses
- Inflammation / blood
- Inflammation / genetics
- Inflammation / veterinary
- Leukocytes / physiology
- RNA / genetics
- RNA / isolation & purification
- Reference Values
- Reverse Transcriptase Polymerase Chain Reaction
- Toll-Like Receptor 4 / genetics
Citations
This article has been cited 3 times.- Taylor S. A review of equine sepsis. Equine Vet Educ 2015 Feb;27(2):99-109.
- Vinther AM, Skovgaard K, Heegaard PM, Andersen PH. Dynamic expression of leukocyte innate immune genes in whole blood from horses with lipopolysaccharide-induced acute systemic inflammation. BMC Vet Res 2015 Jun 16;11:134.
- Lewis DH, Chan DL, Pinheiro D, Armitage-Chan E, Garden OA. The immunopathology of sepsis: pathogen recognition, systemic inflammation, the compensatory anti-inflammatory response, and regulatory T cells. J Vet Intern Med 2012 May-Jun;26(3):457-82.
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