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Background  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. 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.    Methods  BALB/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.    Results  The 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.    Conclusion  These 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

miR-181a regulates the host immune response against Schistosoma japonicum infection through the TLR4 receptor pathway