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Abstract
BackgroundSchistosomiasis japonica is a serious zoonotic parasitic disease. Preliminary studies have shown that the expression of microRNA-181a (miR-181a) in the liver, lung and spleen tissues of susceptible host BALB/c mice and resistant host reed vole (Microtus fortis) 10 days post-infection (dpi) with Schistosoma japonicum was significantly different from pre-infection levels. This difference suggests the possibility that miR-181a expression may be related to the regulation of the hosts’ early immune response against S. japonicum infection and thereby affect the development and survival of parasites in their final hosts.MethodsBALB/c mice, M. fortis, Toll-like receptor 4 (TLR4)-deficient mice and wild-type mice (C57BL/6) were infected with S. japonicum, and differences in miR-181a expression between BALB/c mice and M. fortis over different time points post-infection (0, 3, 7, 10 and 14 dpi) were compared. MiR-181a mimic, miR-181a inhibitor and irrelevant miRNA, as well as lipopolysaccharide (LPS), a TLR4 receptor ligand, were used to transfect mouse RAW264.7 macrophages. The expression levels of the TLR4 pathway-related cytokines interleukin (IL)-1β, tumor necrosis factor α (TNF-α) and IL-6 were detected by quantitative PCR analysis.ResultsThe expression of miR-181a was significantly upregulated in the serum and liver of mice infected with S. japonicum and downregulated in the serum and liver of M. fortis. T-helper cell (Th1)-type cytokines, such as TNF-α, IL-6 and IL-1β, and Th2-type cytokines, such as IL-10 and IL-4, were differentially expressed in M. fortis and BALB/c mice in the early stage of infection. The expression level of miR-181a in the serum was threefold higher in TLR4-deficient mice than in wild-type mice 10 dpi with S. japonicum. The expression of IL-1β, TNF-α and IL-6 decreased in RAW264.7 cells transfected with miR-181a mimic and increased in cells transfected with miR-181a inhibitor. miR-181a expression was downregulated and the expressions of TLR4 and three TLR4 pathway-related cytokines (IL-1β, IL-6, and TNF-α) were upregulated in RAW264.7 macrophages stimulated with the TLR4 receptor ligand LPS.ConclusionThese results suggest the possibility of mutual regulation between miR-181a and the TLR4 signaling pathway during S. japonicum infection. miR-181a may regulate the expression of pro-inflammatory factors through the TLR4 receptor pathway and participate in the immunomodulatory effect of anti-S. japonicum infection.Graphical abstract
Highlights
Schistosomiasis japonica is a serious zoonotic parasitic disease
Analysis of miR‐181a expression in the serum of mice and M. fortis infected with S. japonicum As shown in Fig. 1, the expression of miR-181a in the serum of M. fortis infected with S. japonicum at 3, 7, 10 and 14 dpi, respectively was significantly lower than that in the uninfected control group at the same time points (Fig. 1a)
Analysis of changes in cytokine levels in mice and M. fortis at the early stage of schistosome infection Changes in the expression of cytokines IL-10, IL-4, IL-6, IL-1β and tumor necrosis factor α (TNF-α) were measured in BALB/c mice, the susceptible host of S. japonicum, and in M. fortis, the resistant host, before infection and on 3, 7, 10 and 14 dpi, respectively
Summary
Schistosomiasis japonica is a serious zoonotic parasitic disease. Preliminary studies have shown that the expression of microRNA-181a (miR-181a) in the liver, lung and spleen tissues of susceptible host BALB/c mice and resistant host reed vole (Microtus fortis) 10 days post-infection (dpi) with Schistosoma japonicum was significantly different from pre-infection levels. Studies have shown that during the early period of schistosome infection in mice, the induction of a T-helper cell type I (Th1)-dominated immune response against schistosome infection is characterized by increased levels of interferon-γ (IFN-γ) and tumor necrosis factor α (TNF-α), and that the host immune response shifts to a Th2-dominant immune response 4–6 weeks after infection which is characterized by increased expression levels of several interleukins (ILs), including IL-4, IL-13 and IL-12 [1] Increased expression of these Th1- and Th2-associated cytokines is important in terms of host resistance to schistosome infection. In contrast to M1 macrophages, M2 macrophages are involved in the Th2 bias response, producing transforming growth factor β (TGF-β), IL-10, IL-13 and IL-4, which leads to parasite clearance and host protection [5,6,7]
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