Abstract
Objective Alveolar echinococcosis (AE) is a zoonosis caused by the larval stage of the metacestode Echinococcosis multilocularis with a tumor-like behavior in the targeted organ, especially in the liver. Surgery with albendazole is first-line modality for AE. Drug discontinuation is usually based upon the parasitic viability shown by the positron emission tomography (PET) scan. However, as a demanding and expensive method, it is not widely practiced in majority of the endemic regions. Further understanding on the cytokine and chemokine response profiles in AE patients may provide an interesting insight for potential markers in viability assessment. Methods Mice were inoculated with Echinococcus multilocularis intrahepatically to develop the hepatic AE murine model. Oral albendazole administration was then applied for three months after the first inoculation, and peripheral and regional immune cells including type 1 T helper cells (Th), Th2, Th17, regulatory T (Treg) cells, related cytokines, and chemokines were examined. Results The hepatic AE lesion was confirmed by ultrasound examination resulting in a successful rate of 70%. Among the 17 cytokines and chemokines detected, plasma levels of IL-23 were significantly higher in E. multilocularis-infected mice when compared to the control group; furthermore, more obvious increasing levels were found after albendazole treatment (p < 0.05). All chemokine levels other than eotaxin and MCP-3 were slightly higher in E. multilocularis-infected mice compared to the control group (p > 0.05). Eotaxin levels were significantly decreased in mice with E. multilocularis infection followed by albendazole treatment (p < 0.05). Both IL-17A and IL-23 expressions in hepatic AE lesions were significantly higher and related with disease activity. Conclusion Albendazole administration influenced the balance of immune response and promotes the secretion of proinflammatory factors which is beneficial to parasite clearance. IL-23 seems to be associated with the successful albendazole treatment in mice with E. multilocularis infection; such a change could be translated into clinical application in the near future.
Highlights
Alveolar echinococcosis (AE), a globally distributed zoonotic disease, is caused by the larval stage of the Echinococcus multilocularis metacestode
It is well accepted that 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) is the only diagnostic method evaluating the metabolic activity of AE lesions [5, 6]
We aim to explore the potential influence of albendazole administration on the circulating and regional immune profile in the experimental E. multilocularis infection model and key circulatory markers, if any, that are critical to albendazole administration treatment
Summary
Alveolar echinococcosis (AE), a globally distributed zoonotic disease, is caused by the larval stage of the Echinococcus multilocularis metacestode. Only a few AE patients benefited from radical resection due to the “silent” growth of the parasite and delayed diagnosis, treatment, and BioMed Research International follow-up especially in poorly resourced areas. PET scan determines the boundary of the lesion and assesses metabolic activity It could provide clinicians with a critical reference that was helpful in evaluating the therapeutic effects and optimizing the clinical strategies. For majority of AE patients from poorly resourced areas, it is not readily available. In this background, our previous study pointed out that plasma IL-23 combined with IL-5 could be a marker indicating lesion metabolic activity with similar prognostic values as good as 18F-FDG PET/CT in patients with hepatic AE [7]. We aim to explore the potential influence of albendazole administration on the circulating and regional immune profile in the experimental E. multilocularis infection model and key circulatory markers, if any, that are critical to albendazole administration treatment
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