Abstract
BackgroundCystic echinococcosis is a global parasitic disease caused by infection with Echinococcus granulosus larvae with potentially life-threatening complications in humans. To date, the status of the immune cells believed to be associated with the pathogenicity of E. granulosus infection has not been demonstrated clearly.Methodology/Principal FindingsIn this study, we developed a multiplex flow cytometry assay to investigate the systemic immune status of innate and adaptive immunity at 30, 180, 360 days post-infection (dpi) in mice infected with E. granulousus. At 30 dpi, an increase in the number of CD11b+ and CD11c+ antigen-presenting cells (APCs) was observed. This was accompanied by the slight down-regulated expression of the co-stimulatory molecule MHC-II, indicating the impairment of APCs in early infection through the release of secretory-excretory products. In all infected groups, we observed a significant increase in innate immune cells, including APCs and GR-1+ cells, and a dramatic increase in the myeloid-derived suppressor cells (MDSC) expressing CD11b+/GR-1+. Moreover, the upregulation of the activated markers CD69, CD44, CD40L, and the downregulation of CD62L were observed in the CD4+ and CD8+ T cells following infection. Regulatory T cells expressing CD4+/CD25+/FoxP3 + increased significantly over the course of infection.ConclusionsOur findings demonstrate that the microenvironment in the peripheral immune system after E. granulosus infection changes in subtle but detectably ways, especially during the persistent period of infection. We found that T cells were activated following infection, but observed that the significant increase of immunosuppressive cells such as MDSC and Treg cells could inhibit T cell response to E. granulosus antigens. We suggest these cells may play a neglected but key role in the downregulation of the immune response in long-term parasitic infection. Understanding the basic functions and temporal interactions of these immunosuppressive cells will pave the way for new strategies of parasite vaccine design.
Highlights
Cystic echinococcosis (CE, or hydatid disease) is a chronic endemic helminthic disease caused by infection with metacestodes of the tapeworm Echinococcus granulosus, and is one of the most widespread zoonotic diseases in humans in both developing and developed countries [1,2,3]
Our findings demonstrate that the microenvironment in the peripheral immune system after E. granulosus infection changes in subtle but detectably ways, especially during the persistent period of infection
We found that T cells were activated following infection, but observed that the significant increase of immunosuppressive cells such as myeloid-derived suppressor cells (MDSC) and Treg cells could inhibit T cell response to E. granulosus antigens
Summary
Cystic echinococcosis (CE, or hydatid disease) is a chronic endemic helminthic disease caused by infection with metacestodes (larval stages) of the tapeworm Echinococcus granulosus, and is one of the most widespread zoonotic diseases in humans in both developing and developed countries [1,2,3]. Existing data suggests that the status of innate and adaptive immune cells changes following infection and that these changes are closely related to the pathogenicity of the disease in humans. The status of the innate and adaptive immune cells and their contributions to E. granulosus cyst progression remains poorly understood. Cystic echinococcosis is a global parasitic disease caused by infection with Echinococcus granulosus larvae with potentially life-threatening complications in humans. The status of the immune cells believed to be associated with the pathogenicity of E. granulosus infection has not been demonstrated clearly
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