Heat shock protein 70 protects mouse against post-infection irritable bowel syndrome via up-regulating intestinal γδ T cell’s Th17 response

Abstract

Abstracts Background This study investigated the role of HSP70 in modulating intestinal γδ T cells’ Th17 response in Trichinella spiralis-induced PI-IBS mice model. Methods The intestinal HSP70’s expression and mRNA level were measured by Western blot and RT-PCR. The intestinal γδ T cell’s morphological changes were analyzed using immunofluorescence staining and confocal laser scanning microscope. The pro-inflammatory cytokines’ level was detected by ELISA. The isolated and purified γδ T cells were pre-incubated with HSP70 and their functions including proliferation, apoptosis, activation and production of IL-17 were also detected. Results Heat treatment augmented intestinal HSP70 expression and alleviated the clinical presentations in PI-IBS mice. Meanwhile, intestinal γδ T cells and local IL-17 level were increased by pre-induction of HSP70. HSP70 promoted the proliferation of PI-IBS mice’s intestinal γδ T cells, inhibited the apoptosis and stimulated these cells to secret IL-17 rather than IFN-γ. Conclusion Our results suggest that HSP70 plays a protective role via up-regulating intestinal γδ T cell’s Th17 response in PI-IBS mice.

Keywords

• Heat shock protein 70
• γδ T cells
• Post-infectious irritable bowel syndrome
• Th17 response
• Mice