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Infection by helminthic parasites can cause the polyclonal stimulation of IgE synthesis, possibly via an enhanced production of interleukin-4 (IL-4), and this has been suggested to influence the allergic reactivity of tropical populations where these parasites are endemic. We evaluated a group of urban slum children in Caracas, Venezuela, with a high prevalence of helminthic infection (70.8%), to establish the relationship between the elevated IgE levels (3696 IU/ml) induced by these parasites and various aspects of the allergic response. Although the absolute levels of IL-4 detected in the sera of these children were low (0.65 +/- 0.20 ng/ml), a strong positive correlation (r = 0.78) was found between these and serum IgE. The cutaneous immediate hypersensitivity reactivity to extracts of common environmental allergens was relatively low (17.5% to house dust), although that to Ascaris extract was moderately high (49.4%). Significant inverse correlations were found between total IgE levels and the different skin test reaction diameters, including Ascaris. The positivity of Prausnitz-Kustner passive transfer tests was low in this group (34%), with a strong inverse correlation (r = -0.75) being found between this and total IgE levels. Significant inverse correlations were also found between total IgE levels and specific IgE antibody to environmental allergens, and to Ascaris antigen. We suggest that the polyclonal production of IgE stimulated by helminthic infection can suppress the allergic response to environmental and parasite allergens via both mast cell saturation and inhibition of specific IgE production.

SUMMARYTolal and ^,«-flm-specific serum IgE levels vi^ere measured in a group of 98 Ascaris-infcdcii children from a slum area of Caracas. Venezuela, in whom the infections were eliminated by regular treatment for 22 months with ihe anthelmint O.xantei Pyrantel ('Quanlrel"), The children were re-evalualed at the end of the treatment programme, and then 8 months later, al which lime reinfection was assessed. Total IgE levels at the beginning of the study were significanlly higher in the children who became reinfected after trealmenl. compared with those who did not. The anihclmint treatment caused a significant decrease in Ihe tolal IgE levels in mosl of the children, and afler a period of 8 months without treatment these continued lo decrea.se in the non-reinfected group, bul increased again in Ihe reinfected children. The reverse pattern was found for .'J.vct/r/.v-specific igE antibody levels, and in fad an inverse correlation was found between total and anli-Ascaris IgE levels. Striking associations were found between reinfection and high pretreatment values of lotal IgF.. but low levels of specific IgE antibody. These data support the concept that specific IgE antibody may participale in the protection against helminthic infection, and suggest that Ihe polyclonal stimulation of IgE synthesis caused by these parasites may reduce iheeffeetivenessofsuch responses. The results also indicate that different individuals have varying propensities to respond polyclonally to the helminths, and this influences their resistance lo infeclion.

Helminthic infection can stimulate the interleukin-4 (IL-4)-dependent polyclonal synthesis of immunoglobulin E (IgE) in children endemically exposed to these parasites. As such children are also frequently at nutritional risk, in this study we considered the possible influence of malnutrition on serum IL-4 levels and the IgE response in helminthic infection. We evaluated 85 Ascaris-infected children living in an urban slum area of Caracas, Venezuela, and found that the serum levels of IL-4 and total IgE were significantly higher in malnourished children than in their well nourished counterparts. In contrast, the specific anti-Ascaris IgE antibody response was significantly lower in the malnourished group. After anthelmintic treatment of the children, the total serum IgE and IL-4 levels decreased significantly in the well nourished group, while the specific anti-Ascaris IgE antibody response increased. No significant change was detected, however, in the malnourished group. Our results suggested that malnutrition potentiates the polyclonal stimulation of IgE synthesis induced by helminths. As specific IgE antibody has been implicated in the resistance to helminthic infection, and the polyclonal stimulus diminishes this response, these factors may increase the susceptibility of malnourished children to such parasites.