Cystic echinococcosis is a chronic infectious disease that results from a host/parasite interaction. Vaccination with ferritin derived from Echinococcus granulosus is a potential preventative treatment. To understand whether ferritin is capable of inducing a host immune response, we investigated the response of dendritic cells (DCs) to both recombinant ferritin protein and the hydatid fluid (HF) of E. granulosus. We evaluated the immunomodulatory potential of these antigens by performing, immunocytochemistry, electron microscopy and in vivo imaging of monocyte-derived murine DCs. During antigen stimulation of DCs, ferritin cause DCs maturation and induced higher levels of surface marker expression and activated T-cell proliferation and migration. On contrary, HF failed to induce surface marker expression and to stimulate T-cell proliferation. In response to HF, DCs produced interleukin-6 (IL-6), but no IL-12 and IL-10. DCs stimulated with ferritin produced high levels of cytokines. Overall, HF appears to induce host immunosuppression in order to ensure parasite survival via inhibits DC maturation and promotes Th2-dependent secretion of cytokines. Although ferritin also promoted DC maturation and cytokine release, it also activates CD4+T-cell proliferation, but regard of the mechanism of the Eg.ferritin induce host to eradicate E. granulosus were not clear.
Mice immunized with recombinant Echinococcus granulosus antigens Eg10 and Eg mMDH do not show elevated resistance to E. granulosus infection but show aggravated infection instead. To gain a deeper insight in the immune tolerance mechanisms in mice immunized with Eg10 and Eg mMDH, this study simulated the immune tolerance process in vitro by culturing bone marrow-derived dendritic cells (BMDCs) in the presence of Eg10 or Eg mMDH. Scanning electron microscopy revealed that Eg10- and Eg mMDH-treated DCs exhibited immature cell morphology, while addition of LPS to the cells induced changes in cell morphology and an increase in the number of cell-surface protrusions. This observation was consistent with the increased expression of the cell-surface molecules MHCII and CD80 in Eg10- and Eg mMDH-treated DCs pretreated with LPS. DCs exposed to the two antigens had a very weak ability to induce T-cell proliferation, but could promote the formation of Treg cells. Introduction of the indoleamine 2,3-dioxygenase (IDO) inhibitor, 1-methyl tryptopha (1-MT) enhanced the ability of the antigens to induce T cells and inhibited the induction of Treg cells. Eg mMDH-treated DCs showed a strong response to 1-MT: the DCs had high mRNA levels of IDO, IL-6, and IL-10, while 1-MT decreased the expression. In contrast, DCs treated with Eg10 did not show significant changes after 1-MT treatment. Eg mMDH inhibited DC maturation and promoted IDO expression, which, on the one hand, decreased the ability of DCs to induce T-cell proliferation, resulting in T-cell anergy, and on the other hand, induced the formation of Tregs, resulting in an immunosuppressive effect. In contrast, the escape mechanisms induced by Eg10 did not primarily depend on the IDO pathway and might involve other mechanisms that need to be further explored.
BackgroundBlood gas analyzers (BGAs) and dry biochemistry analyzers for potassium and sodium are based on direct electrode methods, and both involve glucose oxidase for glucose detection. However, data are lacking regarding whether the results of the two assay systems can be used interchangeably. In addition, there remains controversy over the consistency between BGA-measured hemoglobin and complete blood count analyzer data. Here, we compared the consistency of sodium, potassium, glucose, and hemoglobin levels measured by BGA and dry chemistry and complete blood count analyzers.MethodsData from two teaching hospitals, the Zhejiang Provincial People's Hospital (ZRY) and the Qianfoshan Hospital (QY), were retrospectively analyzed based on dry biochemistry and complete blood count analyzer results as the reference system (X) and BGA as the experimental system (Y). Plasma was used for biochemical analysis at the ZRY Hospital, and serum at the QY Hospital. Paired data from the respective hospitals were evaluated for consistency, and biases between methods were assessed by simple correlation, Passing–Bablok regression, and Bland–Altman analyses.ResultsThe correlations of potassium, sodium, glucose, and hemoglobin measured by BGA and dry biochemistry and complete blood count analyzers were high, at 0.9573, 0.8898, 0.9849, and 0.9883 for the ZRY Hospital and 0.9198, 0.8591, 0.9764, and 0.8666, respectively, for the QY Hospital. The results of Passing to Bablok regression analysis showed that the predicted biases at each medical decision level were within clinically acceptable levels for potassium, sodium, glucose, and hemoglobin at the ZRY Hospital. Only the predicted bias of glucose was below the clinically acceptable medical decision levels at the QY Hospital, while potassium, sodium, and hemoglobin were not. Compared with the reference system, the mean bias for BGA measurements at the ZRY Hospital was −0.08 mmol/L (95% confidence interval [CI] −0.091 to −0.069) for potassium, 1.2 mmol/L (95% CI 1.06 to 1.42) for sodium, 0.20 mmol/L (95% CI 0.167 to 0.228) for glucose, and −2.8 g/L for hemoglobin (95% CI −3.14 to −2.49). The mean bias for potassium, sodium, glucose, and hemoglobin at the QY Hospital were −0.46 mmol/L (95% CI −0.475 to −0.452), 3.7 mmol/L (95% CI 3.57 to 3.85), −0.36 mmol/L (95% CI −0.433 to −0.291), and −8.7 g/L (95% CI −9.40 to −8.05), respectively.ConclusionBGA can be used interchangeably with plasma electrolyte results from dry biochemistry analyzers but does not show sufficient consistency with serum electrolyte results from dry biochemistry analyzers to allow data interchangeability. Good consistency was observed between BGA and plasma or serum glucose results from dry biochemistry analyzers. However, BGA-measured hemoglobin and hematocrit assay results should be treated with caution.
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