Background: There is ample evidence that demonstrates a reverse relationship between helminth infection and immune-mediated diseases. Accordingly, several studies have shown that Echinococcus granulosus infection and hydatid cyst compounds are able to suppress immune responses in allergic airway inflammation. Previous studies have documented the ability of hydatid cysts to suppress the aberrant Th2 immune response in allergic asthma’s mouse model. However, there is a paucity of research on the effects of protoscoleces on allergic asthma. Thus, this study was designed to evaluate the effects of somatic antigens of protoscoleces in a murine model of allergic airway inflammation. Methods: Ovalbumin (OVA)/Alum was used to sensitize BALB/c mice intraperitoneally (IP) sensitized over 0 to 7 days and they were then challenged by 1% OVA. The treatment group received somatic antigens of protoscoleces emulsified with PBS on these days in each sensitization before being challenged with 1% OVA on days 14, 15 and 16. The effects of somatic antigens of protoscoleces on allergic airway inflammation were evaluated by examining histopathological changes, the recruitment of inflammatory cells in the bronchoalveolar lavage, cytokines production in the homogenized lung tissue (IL-4, IL-5, IL-10, IL-17 and IFN-γ) and total antioxidant capacity in serum. Results: Overall, the administration of somatic antigens of protoscoleces treatment exacerbated allergic airway inflammation by increasing Th2 cytokines level in the lung homogenate, and recruiting eosinophil into BAL fluid and pathological disorders. In addition, the total antioxidant capacity and IFN-γ levels declined following the administration of somatic antigens. Conclusions: The results revealed that the co-administration of somatic products of protoscoleces with ova-alum contributes to the exacerbation of allergic airway inflammation in BALB/C mice. Currently, the main cause of allergic-type inflammation exacerbation is unknown and further research is needed to understand the mechanism of these interactions.

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