Eosinophils are multifunctional leukocytes, normal constituents of the gastrointestinal tract, except when they are present in the squamous epithelium of the esophagus. Homeostatic eosinophils reside mainly in the lamina propria of the small intestine and protect against parasites and pathogenic bacteria. These cells are selective in their response to the parasites, allowing some to reside in the mucosa, thus regulating the intestinal microbiome and participating in tissue homeostasis.
Eosinophils also modulate the immune response, through the secretion of cytokines that can activate dendritic cells and induce the change of IgA class in B cells. In their homeostatic role, eosinophils are distributed evenly and sparingly within the lamina propria and do not form clusters or suffer degranulation.
In the small intestine, eosinophils maintain IgA levels, by secretory factors that prolong the survival of IgA secreting plasma cells, and induce the production of secretory IgA.
This immunoglobulin is an important first line defense in the mucosa, by preventing the invasion of pathogenic microorganisms by covering them with a hydrophilic envelope that is repelled by the mucosal epithelium, thus allowing the expulsion.
Both tissue and peripheral eosinophilia have been known for a long time as evidence of parasite invasion, and as all pathologists know, when eosinophils predominate in the gastrointestinal mucosa, it is good to consider the principle of “see eosinophils, think about parasites. “
Its excessive presence is not beneficial, as in asthma and eosinophilic gastrointestinal disorders, in which the recruitment of eosinophils is induced by pathogens or allergens, causing epithelial damage.
Primary eosinophilic disorders include esophagitis, gastroenteritis, and eosinophilic colitis. Gastrointestinal involvement can also be observed in the hypereosinophilic syndrome. It is noteworthy that gastroenteritis and eosinophilic colitis are associated with allergic diseases, and frequently, patients have, concurrently, allergies to medications, rhinitis, asthma, sinusitis, dermatitis, food allergies, eczema or urticaria. It has been proven that there are cases of autoimmune connective tissue diseases in patients with eosinophilic gastroenteritis.
The pathogenesis of eosinophilia present in gastroenteritis and eosinophilic colitis is little studied. Histopathology is characterized by an excessive number of eosinophils with signs of degranulation.
The association of allergy and atopy in eosinophilic gastroenteritis and eosinophilic colitis suggests that other allergens may also be responsible in some people, since half of patients with eosinophilic gastritis showed positive skin allergen or allergen skin sensitivity tests , with increased eosinophil count in the blood.
In patients with eosinophilic gastroenteritis and increased expression of the genes involved in the potential operative pathways, a gastric transcriptome was observed, including T-helper immunity driven by interleukins 4, 5 and 13. Some patients with eosinophilic gastrointestinal disorders have a shared autoimmune component without atopy, which could lead to eosinophilia through different immunological pathways, indicating the complexity of this disease.
Gastrointestinal dysbiosis may also play a role in the pathophysiology of these disorders. Alterations in the intestinal microbiota have been implicated in allergy, but it is unknown whether this is a cause or a consequence of the disease.
Patients with eosinophilic gastroenteritis and eosinophilic colitis usually present with nonspecific gastrointestinal symptoms, with a blood eosinophil count that may be normal. Some studies report that the majority of patients (80%) have, at least, mild peripheral eosinophilia.
Gastroenteritis and eosinophilic colitis are often associated with esophageal symptoms of reflux disease, dysphagia and other vague symptoms that include abdominal pain, nausea, vomiting, lack of growth, diarrhea and weight loss. More serious conditions have also been observed: ascites, volvulus, intussusception, perforation and obstruction.
Probably, the clinical presentation depends on the site and the extent and depth of the disease in the gastrointestinal tract. Patients with a more extensive eosinophilic involvement, beyond the mucosa, in the muscle, may present obstruction while those with involvement of the serosa may present with ascites.
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