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Intestinal helminths are among the most common infectious organisms of humans, particularly in tropical regions, and can induce the production of large quantities of IgE antibody. Part of this response is directed against the helminths own antigens, but a polyclonal stimulation also occurs that may increase the allergic reactivity toward environmental allergens. The importance of this in the symptomatology of asthma in these regions is, however, uncertain. In the present study we evaluated the effect of regular anthelminthic treatment with albendazol for 1 yr on a group of asthmatic patients in a zone in which these parasites are endemic. The number of asthmatic crises, need for maintenance therapy with inhaled steroids, and use of inhaled beta 2-agonists were compared both with those in the year prior to the study for the treated patients, and with those in a group of asthmatic subjects evaluated in parallel, but in whom the parasitic infections were not controlled. Significant improvement in all of these indicators of clinical status occurred in the treated group, not only for the period of anthelminth administration, but also for the year following. However, after 2 yr without treatment, the severity of asthma reverted to the initial state. No significant changes were observed in the control group over the entire period of evaluation. At the beginning of the study, the patients' pulmonary function was below the levels predicted for normal individuals, but this was not changed by the anthelminthic treatment. The patients' total serum IgE levels, which were elevated at the beginning of the study, were significantly diminished by the anthelminth administration, as were the specific IgE antibody levels and positivity in skin tests for immediate hypersensitivity to the common environmental allergen Dermatophagoides sp. However, the specific response to Ascaris lumbricoides, a common helminth in the area, was maintained despite treatment. These results indicate that intestinal helminthic infections can contribute to the clinical symptoms of asthma in an endemic situation. This may occur via a direct response to the parasite and/or a nonspecific potentiation of allergic reactivity to environmental allergens.

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The diminishing incidence of parasitic infection in westernised societies has been suggested to result in an increased prevalance of asthma. Asthma is a polygenic disease and genome screens have shown that genes on chromosome 5q31-33 are strongly linked to the disease. The gene for the beta2-adrenoreceptor is located in this region and two polymorphisms have been identified that result in amino acid changes at positions 16 (ArgGly) and 27 (GlnGlu). To determine whether these polymorphisms influence asthma and parasitic infection, a genotype/phenotype study has been performed on a cohort of 126 children from Coche Island in Venezuela. There is a high incidence of asthma on the island and intestinal helminthiasis is endemic. Genotyping for both polymorphisms was carried out by using the polymerase chain reaction and allele-specific oligonucleotide hybridisation. Genotype frequencies in this cohort were consistent with other studies and both polymorphisms were in significant linkage disequilibrium. Individuals who were homozygous for Arg16 had significantly higher levels of specific IgE to Ascaris lumbricoides (P=0.002), significantly higher A. lumbricoides egg counts (P<0.001) and significantly larger wheal sizes following skin-prick testing with A. lumbricoides allergen (P=0.008). There was no association between either polymorphism and total serum IgE or asthma in this population. A combination of mast cell degranulation and the lung migratory phase of A. lumbricoides larvae may result in bronchoconstriction in infected individuals. These results suggest that the Gly 16 allele confers resistance to high levels of parasitic infection in this population. An alternative explanation for the association is that it may be the result of linkage disequilibrium with other genes in the chromosome 5q31-33 region.

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