Schistosomiasis is a serious but neglected tropical infectious disease, afflicting more than 240 million people in 78 countries. Lack of an effective vaccine and obscuring disease mechanism could be the main hurdles to effectively control and eradicate this disease. A better understanding of the host–schistosome interaction is the key to clearing these hurdles. Recently, accumulating evidence shows that alarmin cytokines and microRNAs (miRNAs) are crucial regulators in the host–schistosome interaction. Alarmin cytokines are proven to be potent mechanisms driving type 2 immunity, which is the central disease mechanism of schistosomiasis. MiRNA deregulation is a hallmark of a variety of human diseases, including schistosomiasis. In this review, we summarize the research advances on the role of alarmin cytokines and miRNAs in the host–schistosome interaction.

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Role of alarmin cytokines and microRNAs in the host-schistosome interaction.

Schistosoma mansoni infection decreases IL-33-mRNA expression and increases CXCL9 and CXCL10 production by peripheral blood cells

The host immune response to Schistosoma infection is characterized by two main phases, Th1 and Th2 consecutively, the later one being related to the excretion of mature eggs by the adult female worm. Interleukin-33 (IL-33), a Th2 inducing cytokine, has been reported to be associated with schistosomiasis. Here we assessed the role of this epithelial related cytokine on the time course of the experimental S. mansoni infection in mouse. IL-33 knockout (KO) and wild type (WT) 6-week-old BALB/c female mice were infected with 50 cercariae and sacrificed at 0, 6, 8 and 10 weeks post infection. We monitored symptoms of mice, the worms and eggs burden, kinetics of immune cells in the liver and spleen, and cytokine levels. The size of granuloma induced in the liver and intestine were also measured. There was no significant difference between KO and WT mice in the survival rate, worms and eggs burden; nevertheless some sparse differences related to the increase of eosinophils were detected at 8 weeks post-infection. A very few number of KO mice displayed a severe anemia and colonic bleeding at the end of the experiment, suggesting some intestinal effects of IL-33 as epithelial alarmin. Our results suggest that although IL-33, the Th2 inducing cytokine, was reported to be crucial in other helminthic diseases, it may have little impact on the course of S. mansoni infection.

Eman Sayed

Papers

Role of interleukin-33 during Schistosoma mansoni infection (MPF7P.713)