Abstract
Laboratory zebrafish are commonly infected with the intracellular, brain-infecting microsporidian parasite Pseudoloma neurophilia. Chronic P. neurophilia infections induce inflammation in meninges, brain and spinal cord, and have been suggested to affect neural functions since parasite clusters reside inside neurons. However, underlying neural and immunological mechanisms associated with infection have not been explored. Utilizing RNA-sequencing analysis, we found that P. neurophilia infection upregulated 175 and downregulated 45 genes in the zebrafish brain, compared to uninfected controls. Four biological pathways were enriched by the parasite, all of which were associated with immune function. In addition, 14 gene ontology (GO) terms were enriched, eight of which were associated with immune responses and five with circadian rhythm. Surprisingly, no differentially expressed genes or enriched pathways were specific for nervous system function. Upregulated immune-related genes indicate that the host generally show a pro-inflammatory immune response to infection. On the other hand, we found a general downregulation of immune response genes associated with anti-pathogen functions, suggesting an immune evasion strategy by the parasite. The results reported here provide important information on host-parasite interaction and highlight possible pathways for complex effects of parasite infections on zebrafish phenotypes.
Highlights
Animal research models are crucial for generating new fundamental knowledge in life sciences
We found that the zebrafish immune defence against P. neurophilia appears to be characterized by an upregulation of many immune-related genes and especially a pro-inflammatory T lymphocytes 1 cells (Th1) response
The parasite downregulates genes associated with circadian rhythm, a mechanism often used by parasites to enhance survival
Summary
Animal research models are crucial for generating new fundamental knowledge in life sciences. Studies utilizing animal models can help researchers identify disease mechanisms and develop novel therapeutic agents in human medicine (Insel, 2007). The usefulness of animal models in biological research hinges on study animals being healthy and free of pathogens. Bacteria and parasites are known to influence physiology, immune mechanisms and behaviour, all of which can cause bias in study outcomes (Baker, 1998; Nicklas et al, 1999). Animal research facilities have struggled with pathogen infections since animals were first brought into use by modern science, but concerns about how the spread of pathogens and infectious disease could confound research results were first raised in the mid-1900s (Baker, 2003; Nicklas, 2007).
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