PUBLICATION

Exposure to perfluorooctanoic acid (PFOA) decreases neutrophil migration response to injury in zebrafish embryos

Authors
Pecquet, A.M., Maier, A., Kasper, S., Sumanas, S., Yadav, J.
ID
ZDB-PUB-200902-5
Date
2020
Source
BMC research notes   13: 408 (Journal)
Registered Authors
Sumanas, Saulius
Keywords
Chemotaxis, Immunotoxicity, In situ hybridization, In vivo, Lethal concentration in 50% of embryos (LC50), Myeloperoxidase, Neutrophil, PFOA, Wounding, Zebrafish
MeSH Terms
  • Animals
  • Caprylates/toxicity
  • Fluorocarbons*/toxicity
  • Humans
  • Neutrophils
  • Zebrafish*
PubMed
32867820 Full text @ BMC Res. Notes
Abstract
Perfluorooctanoic acid (PFOA) is a ubiquitous environmental contaminant and a known immune suppressant in humans and experimental animal models. Studies on PFOA have focused on suppression of the adaptive immune response; however, little is known of the impact on innate immunity, especially during embryogenesis. Therefore, we utilized the zebrafish chemotaxis assay coupled with in situ hybridization for myeloperoxidase expression to determine the effects of PFOA exposure on neutrophil migration in the developing zebrafish embryo. Zebrafish embryos are a well-established in vivo model that exhibit high homology with the development of human innate immunity.
Treatment of zebrafish with increasing concentrations of PFOA identified the lethal concentration in 50% of the embryos (LC50) to be 300 mg/L. Utilizing the zebrafish chemotaxis assay, this study showed that wounding induced significant neutrophil migration to the site of injury, and that neutrophil number in the wound region was significantly reduced in response to 48-h PFOA exposure (well below doses causing acute mortality). This study demonstrates that the developing embryo is sensitive to PFOA exposure and that PFOA can modify the innate immune system during embryonic development. These results lay the groundwork for future investigation on the mechanisms underlying PFOA-induced developmental immunotoxicity.
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Human Disease / Model
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