Toxocara (the cause of visceral larva migrans in humans) and allergy have in common both elevated immunoglobulin E (IgE) levels and eosinophilia. In the present study, we investigated: 1) associations between Toxocara seropositivity and allergic manifestations; 2) risk factors for Toxocara infection; and 3) differences in Toxocara seroprevalence, allergic manifestations and the associations between these two, in children from urban and rural environments.Blood samples from 1,379 Dutch urban and rural elementary schoolchildren, were examined for Toxocara antibodies, eosinophil numbers, total IgE concentrations, and the occurrence of inhaled allergen-specific IgE. Questionnaires investigating respiratory health and putative risk factors for infection were completed.It was found that 8% of the children had Toxocara antibodies, occurring significantly less often in females than in males. The means of total serum IgE levels and blood eosinophils were significantly higher in the Toxocara-seropositive than in the seronegative group. Allergic asthma/recurrent bronchitis was found in 7% of the children, allergic reaction on animal contact in 4%, and IgE to at least one inhaled allergen in 16%. These variables were associated with Toxocara seroprevalence. Inhaled allergen-specific IgE and asthma/recurrent bronchitis occurred significantly less often in rural than in urban areas, and significantly less often among girls than among boys. Furthermore, occurrence of allergen-specific IgE increased significantly with age. No association existed between Toxocara seroprevalence and assumed risks, i.e. contact with pet animals and public playgrounds.In conclusion, our results indicate that allergic manifestations occur more often in Toxocara-seropositive children. A relationship with an already existing allergic condition is plausible. Eur Respir J 1997; 10: 1467-1475 Recent investigations suggest an increasing prevalence of childhood asthma [1,2]. Children at risk are those with an atopic constitution [3,4]. The age at which allergy becomes manifest depends mainly on the degree of exposure to inhaled allergens, the most obvious being that to house dust mite (Dermatophagoides pteronyssinus) allergen [5]. Frequent exposure to allergens may accelerate expression of allergic symptoms at a young age [6]. Various products of biological origin, such as antigens derived from parasitic worms, have polyclonal B ε -cell-activating properties, and can, thereby, induce high serum total immunoglobulin E (IgE) concentrations [7,8].Toxocara spp., intestinal parasites of dogs and cats, may spend part of their life cycle in noncompatible hosts, including humans. Toxocara is endemic in the Netherlands. About 8% of the children have antibodies to this roundworm [9]. Eggs are passed on the soil with dog/cat faeces; the infection, therefore, is soil transmitted. Larvae, hatched in the intestine from ingested eggs, migrate to the body tissues, such as liver and lungs. In noncompatible hosts, the larvae do not develop, and may survive as such...
Toxocara seroprevalence and the relation between Toxocara seroprevalence and allergic asthma were investigated in Dutch schoolchildren aged 4-6 years. Data on Toxocara antibodies, allergen-specific immunoglobulin E, allergic manifestations, and risk factors (pets and playgrounds) were obtained from 235 children from The Hague and 477 from Rotterdam, the Netherlands. The surveys were carried out from September 1987 to January 1988 in The Hague and in March and April 1989 in Rotterdam. Logistic regression was used to evaluate putative relations. Toxocara seroprevalence was higher in The Hague (11%) than in Rotterdam (6%), but this difference was not quite significant. Seroprevalences varied widely among schools. No differences between socioeconomic categories or between the sexes were found. Occurrences of asthma/recurrent bronchitis and hospitalization due to asthma/recurrent bronchitis were significantly associated with seroprevalence. Furthermore, a marginally significant relation with eczema was found. Immunoglobulin E specific for inhaled allergens occurred significantly more often in the Toxocara-seropositive group. The risk factors investigated were not related to seroprevalence. It is suggested that Toxocara, among other environmental factors, may stimulate polyclonally immunoglobulin E production, including allergen-specific immunoglobulin E, and thus may contribute to the manifestation of allergic asthma and possibly of eczema in children predisposed to allergy.
The pulmonary immuno-inflammatory reaction and its effect on microvascular integrity was studied in Toxocara canis infected BALB/c mice. The investigation aimed to compare changes in lung histology and composition of bronchoalveolar lavage fluid (BALF) caused by T. canis infection with those described to occur in allergic asthma. Groups of (non)-infected mice (1000 ova) were investigated until 90 days post infection (p.i.). Migration of the larvae through the lungs was followed by a rapidly progressing multifocal interstitial and alveolar inflammation. Eosinophils and lymphocytes formed perivascular and partially peribronchial mixed cellular infiltrates. Lymphocytes with plasma cell morphology staining intracellularly for either alpha, epsilon or gamma immunoglobulins were demonstrated. BALF, collected from mice infected with either 250, 500 or 1000 ova was analysed at 14 and 28 days p.i. A dose-related increase in cell numbers and in albumin and IgA concentration was observed. IgE increase was independent of the infective dose. Peak values were measured at 14 days p.i. Albumin increase in lung homogenate was highest at 28 days p.i. 30% of the lymphocytes consisted of T cells carrying Thy-1,2 and L3T4 surface antigens. It is concluded that T. canis-induced pulmonary inflammation affects the permeability of the microvasculature. This is expressed by interstitial oedema and plasma exudation in the airway lumen. Both phenomena occur also in allergic asthma. It is suggested that increased permeability of the microvasculature is mediated by T cells and eosinophils.
The immunoinflammatory response to parasitic nematode infections and allergic diseases have some similarities, the most profound being the increases in eosinophils and serum total IgE concentration. Whether parasitic infections stimulate or inhibit allergic asthma is a matter of debate. We investigated the effect of Toxocara canis (T. canis) infection on airway function in BALB/c mice at various days post-infection. Within 24 h after infection, the trachea responded hyperreactive to carbachol stimulation. Eosinophils, and to a lesser degree lymphocytes, infiltrated the airways causing interstitial and alveolar inflammation (7 d post-infection). Concurrently with cell infiltration, the trachea became hyporesponsive to carbachol whereas the pulmonary resistance was increased and the dynamic compliance decreased. The hyporeactive response could be simulated in vitro by incubating normal tracheae with eosinophil-enriched bronchoalveolar lavage cells obtained from infected mice. The response depended on the number of cells added to the medium, a lower number causing a hyper- and a higher number a hyporeactive response. Anti-interleukin-5 (anti-IL-5) producing hybridoma cells given simultaneously with T. canis infection inhibited eosinophil infiltration in the airways but not that of lymphocytes. Anti-IL-5 treatment prevented tracheal hyporeactivity but not perivascular and peribronchial edema, increased pulmonary resistance, or decreased dynamic compliance. Treatment with isotype control antibody did not affect eosinophil number nor the observed changes in airway functions. It was concluded that T. canis-induced airway inflammation coincided with increased pulmonary resistance, decreased dynamic compliance, and perivascular/peribronchial edema. These phenomena were independent on the presence of eosinophils, whereas tracheal hyporeactivity was clearly associated with airway eosinophilia.
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