Rat and fish peripheral blood leukocytes respond distinctively to Anisakis pegreffii (Nematoda, Anisakidae) crude extract
Language English Country Switzerland Media electronic-ecollection
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
36590595
PubMed Central
PMC9797851
DOI
10.3389/fcimb.2022.1042679
Knihovny.cz E-resources
- Keywords
- Anisakis, RNA-Seq, crude extract, fish, peripheral blood leukocytes, rat,
- MeSH
- Anisakiasis * veterinary MeSH
- Anisakis * genetics MeSH
- Complex Mixtures MeSH
- Rats MeSH
- Larva MeSH
- Humans MeSH
- Fish Diseases * MeSH
- Fishes MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Complex Mixtures MeSH
Infective third-stage larvae (L3) of the marine nematode Anisakis pegreffii cause inflammation and clinical symptoms in humans, their accidental host, that subside and self-resolve in a couple of weeks after L3 die. To characterise the differences in an early immune response of a marine vs. terrestrial host, we stimulated peripheral blood leukocytes (PBLs) of fish (paratenic host) and rat (accidental, human-model host) with A. pegreffii crude extract and analysed PBL transcriptomes 1 and 12 h post-stimulation. Fish and rat PBLs differentially expressed 712 and 493 transcripts, respectively, between 1 and 12 h post-stimulation (false discovery rate, FDR <0.001, logFC >2). While there was a difference in the highest upregulated transcripts between two time-points, the same Gene Ontologies, biological processes (intracellular signal transduction, DNA-dependent transcription, and DNA-regulated regulation of transcription), and molecular functions (ATP and metal ion binding) were enriched in the two hosts, showing an incrementing dynamic between 1 and 12 h. This suggests that the two distinct hosts employ qualitatively different transcript cascades only to achieve the same effect, at least during an early innate immunity response. Activation of later immunity elements and/or a combination of other host's intrinsic conditions may contribute to the death of L3 in the terrestrial host.
Department of Biology University of Naples Federico 2 Naples Italy
Department of Public Health and Infectious Diseases University of Rome Sapienza Rome Italy
Laboratory of Aquaculture Institute of Oceanography and Fisheries Split Croatia
University Department of Marine Studies University of Split Split Croatia
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