Abstract
BackgroundSoil-transmitted helminths (STH) establish chronic infections in the human intestine. The host reacts to these infections with a dominant T-helper type 2 cell (Th2) response that while attempting to control the worm population, can also provide an anti-inflammatory environment favourable for parasite survival. Regulatory cytokine interleukin 10 (IL-10) has been proposed as a key molecule involved in the attenuation of chronic inflammation and the ensuing tolerance for these helminth parasites. The objective of this study was to determine whether STH-infected children from an endemic community had increased circulating IL-10 levels when compared to non-infected children.ResultsA total of 39 children (25 boys and 14 girls, 7–15 years of age) were enrolled in study. Utilizing the Kato-Katz method to detect intestinal helminthiases, 10 children were non-infected and 29 were harbouring STH infections by Ascaris lumbricoides, Trichuris trichiura and/or hookworms. Of the 29 infected children, 11 had single-species infections and 18 were polyparasitized with two or three STH species. Serum samples from all 39 children were tested for IL-10 serum concentrations, out of which 12 had undetectable levels while 27 had levels ranging from 0.4-105 pg/mL. Excluding extreme outlying values, 25 samples had IL-10 concentration values ranging from 0.4 -7.2 pg/mL. Differences in IL-10 levels among non-parasitized, monoparasitized, and polyparasitized groups were not statistically significant. However, children infected with any of the three STH species investigated had higher IL-10 levels than non-parasitized children (geometric means: 0.89 pg/mL vs. 0.74 pg/mL, p = 0.428). Similarly, polyparasitized children had higher IL-10 levels than both monoparasitized and non-parasitized children (1.04 pg/mL, 0.69 pg/mL, and 0.74 pg/mL, respectively, p = 0.481). A significant moderate negative correlation between IL-10 levels and children’s age was found, but no correlations were observed between IL-10 levels and intensity of infection by any of the parasite species investigated.ConclusionsWe found no strong evidence for an association between STH infection and serum IL-10 concentration levels. However, the trends identified here warrant further investigation. Additional research is needed to expand the current understanding of the immune response elicited by STH infections in children living in endemic communities.
Highlights
Soil-transmitted helminths (STH) establish chronic infections in the human intestine
Because without treatment STH infections are long-lasting and continued re-infection is common, the Th2 polarization is often associated with a regulatory set of cells and cytokines, interleukin 10 (IL-10) and transforming growth factor β (TGF-β), both of which are significantly linked with hyporesponsiveness and susceptibility to infection [15]
To obtain grounds for future investigations, the purpose of this study was to determine whether Honduran children infected with soil-transmitted helminths had higher circulating levels of IL-10 compared to noninfected children
Summary
Soil-transmitted helminths (STH) establish chronic infections in the human intestine. Regulatory cytokine interleukin 10 (IL-10) has been proposed as a key molecule involved in the attenuation of chronic inflammation and the ensuing tolerance for these helminth parasites. Soil-transmitted helminths (STH) are intestinal parasitic nematodes infecting almost 2 billion people worldwide [1]. Knowledge gaps exist regarding the immune mechanisms involved in STH infections [14], it is known that the host-parasite relationship is determined by the interplay of both parasitic manipulation and host tolerance [15] through an efficient induction of a Th2 immune response [16]. Because without treatment STH infections are long-lasting and continued re-infection is common, the Th2 polarization is often associated with a regulatory set of cells and cytokines, IL-10 and transforming growth factor β (TGF-β), both of which are significantly linked with hyporesponsiveness and susceptibility to infection [15]
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