5A). Additional analysis demonstrated that the increase on the anti-Der p1 IgE Index was not associated

with either the intensity of Hookworm or the S. mansoni egg counts ( Fig. 5B). Although several authors have evaluated changes in anti-Der p1 responses following anthelmintic treatment [9,10], in this study we performed comparisons of anti-Der p1 IgE response before and after treatment in all age ranges and in both genders. The populations evaluated had similar age and gender Selleckchem I BET 762 parameters and also allergy risk factors were equally distributed. Treatment against S. mansoni and hookworm was effective in both localities as indicated by negative individuals’ stool egg counts. We also observed that re-infection frequently occurs. Furthermore, we demonstrated that anti-Der p1 IgE levels increased after treatment on population with higher intensity of infection. Worms are known as master pieces on immune regulation and are commonly associated with allergy downregulation. Van den Biggelaar www.selleckchem.com/screening/kinase-inhibitor-library.html and colleagues [10], showed an association between S. mansoni infection and IL-10 production on patient’s serum. IL-10, combined or not with TGF-β, secreted by antigen presenting cells and regulatory T cells may directly interfere with allergic effectors mechanisms by inhibiting mast cell degranulation

or Th2 immune response [ 11, 12]. This mechanism was corroborated in animal models demonstrating that allergic immune response was suppressed

by helminthes and this event was related to increased IL-10 production and regulatory CD4+Foxp3+CD45+ T cells [ 13]. Moreover, it has also been previously shown that PBMC of patients from endemic areas produce lower levels of IL-5 and IL-4 when exposed to Dermatophagoides pteronyssinus antigen (Der p1) than individuals with no helminth infection, resulting in lower levels of anti-Der p1 IgE [ 14]. On the other hand, worm antigens exposure stimulated by anthelmintic therapy promotes an increase of IL-5 and IL-4 productions [ 15, 16]. At the same time, IL-10 production is suppressed, what may lead to IgE production including IgE anti-Der p1 [ 17, 18]. In vitro studies demonstrate that Praziquantel can alter worm tegument; liberating or exposing inner worm antigens can also stimulate IL-6, TNF-α and eotaxin production culminating ID-8 in antibodies isotypes changes over weeks or months [ 12, [19], [20], [21] and [22]]. Our data also support these findings as we showed that anti-Derp1 IgE levels increase after treatment. We propose that this might be related to decreased IL-10 resulting in increased IL-4 production. Concerning geohelminths, it has been demonstrated that Albendazole treatment was strongly associated with recurrent wheeze [21]. Moreover, it was observed that Albendole treatment during pregnancy enhances infantile eczema [23] and also increases in anti-Der p1 IgE [24,25].