Abstract
It is well known that eosinophilia is a key pathogenetic component of toxocariasis. The objective of the present study was to determine if there is an association between peritoneal and blood eosinophil influx, mast cell hyperplasia and leukotriene B4 (LTB4) production after Toxocara canis infection. Oral inoculation of 56-day-old Wistar rats (N = 5-7 per group) with 1000 embryonated eggs containing third-stage (L3) T. canis larvae led to a robust accumulation of total leukocytes in blood beginning on day 3 and peaking on day 18, mainly characterized by eosinophils and accompanied by higher serum LTB4 levels. At that time, we also noted increased eosinophil numbers in the peritoneal cavity. In addition, we observed increased peritoneal mast cell number in the peritoneal cavity, which correlated with the time course of eosinophilia during toxocariasis. We also demonstrated that mast cell hyperplasia in the intestines and lungs began soon after the T. canis larvae migrated to these compartments, reaching maximal levels on day 24, which correlated with the complete elimination of the parasite. Therefore, mast cells appear to be involved in peritoneal and blood eosinophil infiltration through an LTB4-dependent mechanism following T. canis infection in rats. Our data also demonstrate a tight association between larval migratory stages and intestinal and pulmonary mast cell hyperplasia in the toxocariasis model.
Highlights
Intestinal nematodes cause some of the most prevalent parasitic infections in humans
Three major effects were observed: 1) increased peripheral blood and tissue eosinophil influx and eosinophil peroxidase (EPO) activity, 2) significant peritoneal mast cell accumulation and leukotriene B4 (LTB4) production in the serum following T. canis infection, and 3) mast cell hyperplasia in the lungs and intestinal tissues probably induced by the passage of larvae into these compartments
Increased eosinophilia was observed in the blood and peritoneal cavities of rats infected with T. canis
Summary
Intestinal nematodes cause some of the most prevalent parasitic infections in humans. Toxocara canis is an intestinal parasite of dogs, and is the etiologic agent of visceral larva migrans syndrome (VLMS). In non-compatible hosts such as rodents and humans, VLMS results from the ingestion of T. canis-embryonated eggs that eclode in the small intestine. The larvae migrate to other tissues, inducing inflammation in reaction to the excretory/secretory products produced by the larvae [1]. Helminthic parasites infect vertebrate hosts and typically promote a Th2-type inflammatory response that is marked by eosinophilia, high levels of immunoglobulin E (IgE) and mast cell hyperplasia [2]. Studies from our laboratory have shown an accumulation of eosinophils and increased total serum
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