Transcriptome study reveals tick immune genes restrict Babesia microti infection.
Tingting FengHao TongFeihu ZhangQianqian ZhangHeng ZhangXia ZhouHang RuanQihan WuJianfeng DaiPublished in: Insect science (2024)
A systems biology approach was employed to gain insight into tick biology and interactions between vectors and pathogens. Haemaphysalis longicornis serves as one of the primary vectors of Babesia microti, significantly impacting human and animal health. Obtaining more information about their relationship is crucial for a comprehensive understanding of tick and pathogen biology, pathogen transmission dynamics, and potential control strategies. RNA sequencing of uninfected and B. microti-infected ticks resulted in the identification of 15 056 unigenes. Among these, 1 051 were found to be differentially expressed, with 796 being upregulated and 255 downregulated (P < 0.05). Integrated transcriptomics datasets revealed the pivotal role of immune-related pathways, including the Toll, Janus kinase/signal transducer and activator of transcription (JAK-STAT), immunodeficiency, and RNA interference (RNAi) pathways, in response to infection. Consequently, 3 genes encoding critical transcriptional factor Dorsal, Relish, and STAT were selected for RNAi experiments. The knockdown of Dorsal, Relish, and STAT resulted in a substantial increase in Babesia infection levels compared to the respective controls. These findings significantly advanced our understanding of tick-Babesia molecular interactions and proposed novel tick antigens as potential vaccine targets against tick infestations and pathogen transmission.
Keyphrases
- single cell
- genome wide
- rna seq
- spinal cord
- gene expression
- bioinformatics analysis
- candida albicans
- cell proliferation
- neuropathic pain
- public health
- dna methylation
- mental health
- transcription factor
- spinal cord injury
- tyrosine kinase
- single molecule
- gene therapy
- health information
- multidrug resistant
- inflammatory response
- oxidative stress
- protein kinase
- antimicrobial resistance
- drug induced