In areas where schistosomiasis is endemic, a negative correlation is observed 
between atopy and helminth infection, associated with a low prevalence of 
asthma. We investigated whether Schistosoma mansoni infection or injection of 
parasite eggs can modulate airway allergic inflammation in mice, examining the 
mechanisms of such regulation. We infected BALB/c mice with 30 S. mansoni 
cercariae or intraperitoneally injected 2,500 schistosome eggs, and experimental 
asthma was induced by ovalbumin (OVA). The number of eosinophils in 
bronchoalveolar lavage fluid was higher in the asthmatic group than in asthmatic 
mice infected with S. mansoni or treated with parasite eggs. Reduced Th2 
cytokine production, characterized by lower levels of interleukin-4 (IL-4), 
IL-5, and immunoglobulin E, was observed in both S. mansoni-treated groups 
compared to the asthmatic group. There was a reduction in the number of 
inflammatory cells in lungs of S. mansoni-infected and egg-treated mice, 
demonstrating that both S. mansoni infection and the egg treatment modulated the 
lung inflammatory response to OVA. Only allergic animals that were treated with 
parasite eggs had increased numbers of CD4(+) CD25(+) Foxp3(+) T cells and 
increased levels of IL-10 and decreased production of CCL2, CCL3, and CCL5 in 
the lungs compared to the asthmatic group. Neutralization of IL-10 receptor or 
depletion of CD25(+) T cells in vivo confirmed the critical role of CD4(+) 
CD25(+) Foxp3(+) regulatory T cells in experimental asthma modulation 
independent of IL-10.