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Microtus fortis  exhibits natural resistance against  Schistosoma japonicum , and the parasite cannot grow and develop in  M. fortis . Extensive research has been carried out, however, the associated mechanism remains unclear. In the present study, we analysed the combined data obtained from a cytokine chip assay, transcriptome, and metabolome. The cytokine profile from C57BL/6 and  M. fortis  mice was assessed before and after infection. Several cytokines increased during the second and third week post-infection. Some transcripts related to cytokine genes and associated proteins were also highly expressed (i.e.,  Hgf, C3 , and  Lbp ). The liver metabolism of  M. fortis  following infection with  S. japonicum  was assessed. We identified 25 different metabolites between the uninfected and infected  M. fortis , and 22 different metabolites between infected  M. fortis  and C57BL/6 mice. The metabolomic pathways of these differential metabolites were then analysed with MetPA, revealing that they were involved in histidine metabolism, valine, leucine, and isoleucine biosyntheses, and lysine degradation. Thus, the elevated expression of these metabolites and pathways may promote the phagocytic function of the neutrophils and natural killer cell activity following TLR activation. These results provide novel insight into the resistance mechanism of  M. fortis  against  S. japonicum .

High throughput data analyses of the immune characteristics of Microtus fortis infected with Schistosoma japonicum