Schistosoma japonicum peptide SJMHE1 suppresses airway inflammation of allergic asthma in mice

J Cell Mol Med. 2019 Nov;23(11):7819-7829. doi: 10.1111/jcmm.14661. Epub 2019 Sep 9.


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.

Keywords: SJMHE1; Schistosoma japonicum peptide; airway inflammation; allergic asthma; suppress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Asthma / complications
  • Asthma / drug therapy*
  • Asthma / immunology
  • Asthma / pathology
  • Cytokines / genetics
  • Cytokines / metabolism
  • Forkhead Transcription Factors / metabolism
  • GATA3 Transcription Factor / genetics
  • GATA3 Transcription Factor / metabolism
  • Gene Expression Regulation / drug effects
  • Hypersensitivity / complications
  • Hypersensitivity / drug therapy*
  • Hypersensitivity / immunology
  • Hypersensitivity / pathology
  • Inflammation / complications
  • Inflammation / drug therapy*
  • Inflammation / immunology
  • Inflammation / pathology
  • Lung / pathology*
  • Lymphocyte Subsets / drug effects
  • Lymphocyte Subsets / immunology
  • Mice
  • Mice, Inbred BALB C
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / genetics
  • Nuclear Receptor Subfamily 1, Group F, Member 3 / metabolism
  • Ovalbumin / immunology
  • Peptides / pharmacology
  • Peptides / therapeutic use*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Schistosoma japonicum / chemistry*
  • Spleen / drug effects
  • Spleen / metabolism
  • T-Box Domain Proteins / genetics
  • T-Box Domain Proteins / metabolism


  • Cytokines
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • GATA3 Transcription Factor
  • Nuclear Receptor Subfamily 1, Group F, Member 3
  • Peptides
  • RNA, Messenger
  • Rorc protein, mouse
  • T-Box Domain Proteins
  • T-box transcription factor TBX21
  • Ovalbumin