Abstract
BackgroundPrevious studies have demonstrated that S. mansoni infection and inoculation of the parasite eggs and antigens are able to modulate airways inflammation induced by OVA in mice. This modulation was associated to an enhanced production of interleukin-10 and to an increased number of regulatory T cells. The S. mansoni schistosomulum is the first stage to come into contact with the host immune system and its tegument represents the host-parasite interface. The schistosomula tegument (Smteg) has never been studied in the context of modulation of inflammatory disorders, although immune evasion mechanisms take place in this phase of infection to guarantee the persistence of the parasite in the host.Methodology and Principal FindingsThe aim of this study was to evaluate the Smteg ability to modulate inflammation in an experimental airway inflammation model induced by OVA and to characterize the immune factors involved in this modulation. To achieve the objective, BALB/c mice were sensitized with ovalbumin (OVA) and then challenged with OVA aerosol after Smteg intraperitoneal inoculation. Protein extravasation and inflammatory cells were assessed in bronchoalveolar lavage and IgE levels were measured in serum. Additionally, lungs were excised for histopathological analyses, cytokine measurement and characterization of the cell populations. Inoculation with Smteg led to a reduction in the protein levels in bronchoalveolar lavage (BAL) and eosinophils in both BAL and lung tissue. In the lung tissue there was a reduction in inflammatory cells and collagen deposition as well as in IL-5, IL-13, IL-25 and CCL11 levels. Additionally, a decrease in specific anti-OVA IgE levels was observed. The reduction observed in these inflammatory parameters was associated with increased levels of IL-10 in lung tissues. Furthermore, Smteg/asthma mice showed high percentage of CD11b+F4/80+IL-10+ and CD11c+CD11b+IL-10+ cells in lungs.ConclusionTaken together, these findings demonstrate that S. mansoni schistosomula tegument can modulates experimental airway inflammation.
Highlights
Asthma is characterized by chronic inflammation of the airways and lungs with marked Th2 response, as showed by high concentrations of interleukin (IL)-4, IL-5 and IL-13, IgE production, mucus and eosinophils influx to airways [1]
Smteg/asthma mice showed high percentage of CD11b+F4/ 80+IL-10+ and CD11c+CD11b+IL-10+ cells in lungs. These findings demonstrate that S. mansoni schistosomula tegument can modulates experimental airway inflammation
We demonstrated the ability of Smteg to modulate the experimental airway inflammation induced by OVA, downregulating inflammatory parameters such as number of eosinophils, proinflammatory cytokines, specific anti-OVA IgE and lung pathology
Summary
Asthma is characterized by chronic inflammation of the airways and lungs with marked Th2 response, as showed by high concentrations of interleukin (IL)-4, IL-5 and IL-13, IgE production, mucus and eosinophils influx to airways [1]. It is a global health problem that affects people of all ages worldwide and its prevalence is increasing in several countries, especially among children It is the commonest cause of medical admission in childhood and has a major impact on hospital services for adults [2,3,4,5]. Previous studies have demonstrated that S. mansoni infection and inoculation of the parasite eggs and antigens are able to modulate airways inflammation induced by OVA in mice. This modulation was associated to an enhanced production of interleukin-10 and to an increased number of regulatory T cells. The schistosomula tegument (Smteg) has never been studied in the context of modulation of inflammatory disorders, immune evasion mechanisms take place in this phase of infection to guarantee the persistence of the parasite in the host
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