The eosinophilic granulocyte is a resident cell of gastrointestinal lamina propria, but to date, the precise function of this cell under resting or inflammatory conditions is not clearly understood.1,2 Eosinophils can be distinguished from other leukocytes by their unique granule populations, which include unicompartmental primary granules, bicompartmental secondary granules that consist of a matrix and a crystalloid core, and lipid bodies that are prominent organelles of the mature eosinophil.2 The only nonhematopoietic organ with resident eosinophils under resting conditions is the gastrointestinal tract.3 In humans that do not have alimentary tract disease, the cecal and appendiceal regions have the highest density of eosinophils and the esophagus is the only segment of the gastrointestinal tract without resident eosinophils.4 Within the gastrointestinal tract in humans, the eosinophil resides almost exclusively in the lamina propria compartment, close to the muscularis mucosae.1
Eosinophils develop from hematopoietic stem cells under the influence of IL-5, IL-3, and GM-CSF.5 Eotaxin-1 is the primary regulator of homing of eosinophils into the gastrointestinal tract. Homing occurs during the embryonic development and is independent of the presence of intestinal flora in mice.6 To date, many inflammatory mediators have been implicated in regulating eosinophil accumulation, but only IL-5 and eotaxin are somewhat specific for eosinophils.7 In horses, eotaxin-1 mRNA was found to be strongly expressed in the jejunum and colon,8 and the authors suggested that his could explain why the normal equine gastrointestinal mucosa had large numbers of resident eosinophils, compared with other equine tissues (eg, skin, lung, liver, spleen, and kidney).8
Eosinophils are proinflammatory leukocytes with a wide range of functions. In humans with eosinophilic gastroenteritis, eosinophils can be found in all levels of the affected mucosa9 and a correlation exists between degree of eosinophil accumulation and disease severity.10–12 Clinically affected horses with focal and diffuse eosinophilic gastroenteritis have been reported, and clinical signs include weight loss, diarrhea, signs of depression, acute and chronic colic, and hypoalbuminemia.13–16 The predominant histopathologic findings in these affected horses are severe mural inflammation in which eosinophilic leukocytes are the predominant inflammatory cell.17–19 The cause of eosinophil accumulation is unknown in these horses and has been attributed to immune-mediated processes, such as food allergy or parasite infection. Horses with focal eosinophilic enteritis often respond well to surgical removal of diseased intestinal segments.18,19 Furthermore, accumulation of eosinophils has been described for horses with experimentally induced acute colitis20 and in horses with experimentally induced ischemia and reperfusion injury.21 Eosinophil accumulation in the gastrointestinal mucosa can also be associated with parasitism.22 Another eosinophil-associated disease in horses is MEED.23–25 This disease is characterized by eosinophilic infiltrates in various tissues, most commonly the gastrointestinal tract, respiratory tract, and skin as well as the pancreas, biliary epithelium, and salivary glands.23,25 Clinical signs of MEED vary depending on the degree of involvement of these systems but often include weight loss and skin lesions.23,25 Multisystemic eosinophilic epitheliotropic disease affects mostly young horses between the ages of 3 to 13 years, and prognosis for survival is poor.24,25 The etiology of MEED is unknown, and parasitic, allergic, toxic, and viral causes have been suggested.24
To date, the authors have found no reference range information on the numbers of eosinophils and their distribution in the gastrointestinal mucosa of healthy horses. The goals of the study reported here were to establish these reference values for eosinophils and to describe the distribution of this cell within the equine gastrointestinal mucosa.
Granulocyte macrophage colony-stimulating factor
Multisystemic eosinophilic epitheliotropic disease
Image Pro Express, version 4.5, Media Cybernetics Inc, Bethesda, Md.
PROC MIXED, SAS, version 9.1, SAS Institute Inc, Cary, NC.
Straumann A, Simon HU. The physiological and pathophysiological roles of eosinophils in the gastrointestinal tract. Allergy 2004;59:15–25.
Kato M, Kephart GM, Talley NJ, et al. Eosinophil infiltration and degranulation in normal human tissue. Anat Rec 1998;252:418–425.
Lowichik A, Weinberg AG. A quantitative evaluation of mucosal eosinophils in the pediatric gastrointestinal tract. Mod Pathol 1996;9:110–114.
Sehmi R, Denburg J. Differentiation of human eosinophils. In: Marone G, ed. Human eosinophils, biological and clinical aspects. Basel, Switzerland: Karger, 2000;76:29–44.
Mishra A, Hogan SP, Lee JJ, et al. Fundamental signals that regulate eosinophil homing to the gastrointestinal tract. J Clin Invest 1999;103:1719–1727.
Benarafa C, Cunningham FM, Hamblin AS, et al. Cloning of equine chemokines eotaxin, monocyte chemoattractant protein (MCP)-1, MCP-2 and MCP-4, mRNA expression in tissues and induction by IL-4 in dermal fibroblasts. Vet Immunol Immunopathol 2000;76:283–298.
Desreumaux P, Bloget F, Seguy D, et al. Interleukin 3, granulocyte-macophage colony-stimulating factor, and interleukin 5 in eosinophilic gastroenteritis. Gastroenterology 1996;110:768–774.
Torpier G, Colombel JF, Mathieu-Chandelier C, et al. Eosinophilic gastroenteritis: ultrastructural evidence for a selective release of eosinophil major basic protein. Clin Exp Immunol 1988;74:404–408.
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Stanar LS, Little D, Redding WR, et al. Idiopathic eosinophilic enteritis in a 10-week-old colt. Compend Contin Educ Pract Vet 2002;24:342–347.
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Morton LD, Morton DG, Baker GJ, et al. Chronic eosinophilic enteritis attributed to Pythium sp. in a horse. Vet Pathol 1991;28:542–544.
Archer DC, Edwards GB, Kelly DF, et al. Obstruction of equine small intestine associated with focal idiopathic eosinophilic enteritis: an emerging disease. Vet J 2006;171:504–512.
Southwood LL, Kawcak CE, Trotter GW, et al. Idiopathic focal eosinophilic enteritis associated with small intestinal obstruction in 6 horses. Vet Surg 2000;29:415–419.
McConnico RS, Weinstock D, Poston ME, et al. Myeloperoxidase activity of the large intestine in an equine model of acute colitis. Am J Vet Res 1999;60:807–813.
Moore RM, Bertone AL, Bailey MQ, et al. Neutrophil accumulation in the large colon of horses during low-flow ischemia and reperfusion. Am J Vet Res 1994;55:1454–1463.
Collobert-Laugier C, Hoste H, Sevin C, et al. Mast cell and eosinophil mucosal responses in the large intestine of horses naturally infected with cyathostomes. Vet Parasitol 2002;107:251–264.
Henson FMD, Milner PI, Sheldon O. Multisystemic eosinophilic epitheliotrophic disease in a Welsh pony. Equine Vet Educ 2002;224–226.
La Perle KMD, Piercy RJ, Long JF, et al. Mutisystemic, eosinophilic, epitheliotropic disease with intestinal lymphosarcoma in a horse. Vet Pathol 1998;35:144–146.
McCue ME, Davis EG, Rush BR, et al. Dexamethasone for treatment of multisystemic eosinophilic epitheliotropic disease in a horse. J Am Vet Med Assoc 2003;223:1320–1323.
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Rötting AK, Freeman DE, Eurell JA, et al. Effects of acetylcysteine and migration of resident eosinophils in an in vitro model of mucosal injury and restitution in equine right dorsal colon. Am J Vet Res 2003;64:1205–1212.
Moore RM, Bertone AL, Muir WW, et al. Histopathologic evidence of reperfusion injury in the large colon of horses after low-flow ischemia. Am J Vet Res 1994;55:1434–1443.
Packer M, Patterson-Kane JC, Smith KC, et al. Quantification of immune cell populations in the lamina propria of equine jejunal biopsy specimens. J Comp Pathol 2005;132:90–95.
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Collobert-Laugier C, Hoste H, Sevin C, et al. Prevalence, abundance and site distribution of equine small strongyles in Normandy, France. Vet Parasitol 2002;110:77–83.