Abstract
BackgroundThere is ample evidence demonstrating 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 aberrant Th2 immune response in a mouse model of allergic asthma. 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.MethodsOvalbumin (OVA)/aluminum hydroxide (alum) was injected intraperitoneally to sensitize BALB/c mice over a period of 0 to 7 days, followed by challenge with 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, cytokine production in the homogenized lung tissue (IL-4, IL-5, IL-10, IL-17, and IFN-γ), and total antioxidant capacity in serum.ResultsOverall, administration of somatic antigens of protoscoleces exacerbated allergic airway inflammation via increased Th2 cytokine levels in the lung homogenate, recruitment of eosinophils into bronchoalveolar lavage fluid, and pathological changes. In addition, total antioxidant capacity and IFN-γ levels declined following the administration of somatic antigens.ConclusionsThe results revealed that the co-administration of somatic products of protoscoleces with OVA/alum contributed 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.Graphical
Highlights
There is ample evidence demonstrating a reverse relationship between helminth infection and immune-mediated diseases
The results revealed that laminated layer extracts (LLs) reduced nitric oxide (NO) production in patients with severe asthma [11]
The results of differential cell counting of cells in the bronchoalveolar lavage fluid (BALF) showed that mice receiving OVA + antigen exhibited a dramatic increase in the total cell count in the BALF, and the predominant cells were eosinophils
Summary
There is ample evidence demonstrating a reverse relationship between helminth infection and immune-mediated diseases. 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 aberrant Th2 immune response in a mouse model of allergic asthma. This study was designed to evaluate the effects of somatic antigens of protoscoleces in a murine model of allergic airway inflammation. As shown by in vivo experiments, E. granulosus infection dramatically decreases the airway inflammation induced by ovalbumin (OVA) by increasing interleukin 10 (IL-10) and downregulating IL-5 and IL-17A in serum and lung tissues [10]. Immunomodulatory molecules (IMs) in the hydatid cystic fluid have therapeutic potential for suppressing allergic airway inflammation by modifying immune cell activation and cytokine balance through a surge in CD4+CD25+Foxp3+ T cells (Treg cells) [12]
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