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Transcriptional profiling of Microtus fortis responses to S. japonicum : New sight into Mf‐Hsp90 α resistance mechanism
Author(s) -
Xiong Dehui,
Luo Saiqun,
Wu Kunlu,
Yu Yuanjing,
Sun Jiameng,
Wang Yanpeng,
Hu Jingping,
Hu Weixin
Publication year - 2021
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12842
Subject(s) - schistosoma japonicum , kegg , biology , transcriptome , hsp90 , gene , virology , heat shock protein , genetics , schistosomiasis , immunology , gene expression , helminths
Aims Schistosomiasis is a parasitic disease with a chronic debilitating character caused by parasitic flatworms of the genus Schistosoma . The main disease‐causing species of Schistosoma in China is S. japonicum . M fortis has been proved to be a nonpermissive host of S. japonicum . Mf‐HSP90 α ( Microtus fortis heat shock protein 90alpha), the homologue of HSP90 α , display anti‐schistosome effect in vitro and in vivo. In the current study, in order to investigate the mechanism of anti‐schistosome effect of Mf‐HSP90 α , we conducted RNA‐Seq to obtain the transcriptome profile of M. fortis liver infected with S. japonicum at different time points. Methods and Results By mapping the differential expressed genes (DEGs) to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), we found that the JAK2/STAT1 pathway was highly enriched with an elevated level of IL‐10 and HSP90 α . We then checked the IL‐10‐JAK2/STAT1‐HSP90 α pathway, and found that this pathway was activated in the infected mice with S. japonicum . The expression of the molecules in this pathway was elevated on the 10 th day after infection and gradually decreased on the 20 th day. Conclusions The IL‐10‐JAK2/STAT1‐HSP90 α axis was associated with the anti‐schistosome effect of Mf‐HSP90 α , and targeting IL‐10‐JAK2/STAT1‐HSP90 α axis might be a novel therapeutic strategy for developing resistance to S. japonicum infection.