Helminths and their products can shape immune responses by modulating immune 
cells, which are dysfunctional in inflammatory diseases such as asthma. We 
previously identified SJMHE1, a small molecule peptide from the HSP60 protein of 
Schistosoma japonicum. SJMHE1 can inhibit delayed-type hypersensitivity and 
collagen-induced arthritis in mice. In the present study, we evaluated this 
peptide's potential intervention effect and mechanism on ovalbumin-induced 
asthma in mice. SJMHE1 treatment suppressed airway inflammation in allergic 
mice, decreased the infiltrating inflammatory cells in the lungs and 
bronchoalveolar lavage fluid, modulated the production of pro-inflammatory and 
anti-inflammatory cytokines in the splenocytes and lungs of allergic mice, 
reduced the percentage of Th2 cells and increased the proportion of Th1 and 
regulatory T cells (Tregs). At the same time, Foxp3 and T-bet expression 
increased, and GATA3 and RORγt decreased in the lungs of allergic mice. We 
proved that SJMHE1 can interrupt the development of asthma by diminishing airway 
inflammation in mice. The down-regulation of Th2 response and the up-regulation 
of Th1 and Tregs response may contribute to the protection induced by SJMHE1 in 
allergic mice. SJMHE1 can serve as a novel therapy for asthma and other allergic 
or inflammatory diseases.