Abstract
BackgroundCystic echinococcosis (CE) is a worldwide parasitic zoonosis caused by infection of the larval stage of tapeworm Echinococcus granulosus. In human CE, the parasites develop and form cysts in internal organs. The differentiated cysts can be classified into five types based on WHO-IWGE standard CE1-5 representing different developmental stages. Infection with E. granulosus triggers hosts’ humoral and cellular response, displaying elevated serum antibodies and Th1 and Th2 cytokines, which are presumed to be in association with the disease outcome. Identification of immunological markers for evaluation of disease progression has been a growing concern. However, the distinctive profile of cytokines and antibodies associated with the cyst progression has not been ascertained.MethodsTo better understand the interaction between host immune response and disease outcome, the present study followed-up four CE patients over three years by yearly measuring serum level of 27 cytokines, total IgG and isotypes, and ultrasound scanning, beginning in year 1 for all patients with CE1 and CE2 cysts before treatment and continued in year 2 with CE4 and in year 3 with CE3-CE5 post-treatment.ResultsNine cytokines including Th1-type IL-2, Th17-type IL-17A, and inflammatory cytokines IL-1β, IL-1Rα and TNF-α, chemokines IL-8, MIP-1α, MIP-1β, and growth factor G-CSF were significantly elevated in patients with cyst type CE1, compared to the normal controls, and then declined to a normal level at CE4 and CE5. Examining the antibody production, we found that serum specific IgG was significantly increased in patients with active and transitional cysts, specifically the total IgG at CE1/CE3/CE4-CE5, IgG4 at CE1 and IgG1 at CE1/CE3 cyst status, in comparison with the normal controls, but showed no significant changes between the cyst stages.ConclusionsOur findings provide new information on the profile of multiplex cytokines and serum antibodies associated with cyst stages in cystic echinococcosis patients through a three-year follow-up, implying that further studies using an approach combining cyst-associated immune parameters may aid in identifying immunological markers for differentiation of disease progression.
Highlights
Cystic echinococcosis (CE) is a worldwide parasitic zoonosis caused by infection of the larval stage of tapeworm Echinococcus granulosus
We noted that the levels of nine cytokines including T helper cell 1 (Th1)-type IL-2, Th17-type IL-17A, and inflammatory cytokines IL-1β, interleukin-1 receptor antago‐ nist (IL-1Rα) and TNFα, chemokines IL-8, macrophage inflammatory protein-1α (MIP-1α), and macrophage inflammatory protein-1β (MIP-1β), and growth factor G-CSF were significantly elevated in patients with cyst type CE1, compared to the normal controls; the level of these cytokines decreased to around the normal range in patients with CE4 and CE5 (P < 0.01–0.0001); among these cytokines, IL-1β, IL-8, MIP-1α and G-CSF presented the highest concentration (P < 0.0001, Fig. 2)
Our findings present several noticeable facets: (i) our findings are in agreement with the general understanding that the immune response to hydatid cysts in intermediate hosts is a complex and contradictory issue, the imbalance of Th1/T helper cell 2 (Th2) plays an important role in promoting the immunopathogenesis change of this disease via cytokine Th1-type IFN-γ and Th2-type IL-4 [20, 21]; (ii) we found elevated Th1-type and other cytokine types in patients with active cysts (CE1) before treatment compared with the normal controls, but no measurable shift
Summary
Cystic echinococcosis (CE) is a worldwide parasitic zoonosis caused by infection of the larval stage of tapeworm Echinococcus granulosus. Infection with E. granulosus triggers hosts’ humoral and cellular response, displaying elevated serum antibodies and Th1 and Th2 cytokines, which are presumed to be in association with the disease outcome. Cystic echinococcosis (CE), called hydatid disease, is a serious parasitic zoonosis with a worldwide distribution, caused by the larval stage of the cestode Echinococcus granulosus. In humans and other intermediate hosts, the parasites develop and form cysts in internal organs, especially the liver (70% cases) and the lungs (20% cases), manifesting slow-growing, space-occupying lesions, which may lead to severe consequences and can be potentially lethal if not diagnosed and treated timely and appropriately [3,4,5,6]. Infection of E. granulosus in humans triggers humoral and cellular response, displaying elevated serum antibodies and T helper cell 1 (Th1) and T helper cell 2 (Th2) cytokines. A very recent experimental infection study found similar dynamic patterns that supports the shift of immune response from Th1 to Th2 [12]
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