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Neurological infection, kynurenine pathway, and parasitic infection by Neospora caninum

Ana Elisa Del’Arco, Deivison Silva Argolo, Gilles Guillemin, Maria de Fátima Dias Costa, Silvia Lima Costa, Alexandre Moraes Pinheiro*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

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Abstract

Neuroinflammation is one of the most frequently studied topics of neurosciences as it is a common feature in almost all neurological disorders. Although the primary function of neuroinflammation is to protect the nervous system from an insult, the complex and sequential response of activated glial cells can lead to neurological damage. Depending on the type of insults and the time post-insult, the inflammatory response can be neuroprotective, neurotoxic, or, depending on the glial cell types, both. There are multiple pathways activated and many bioactive intermediates are released during neuroinflammation. One of the most common one is the kynurenine pathway, catabolizing tryptophan, which is involved in immune regulation, neuroprotection, and neurotoxicity. Different models have been used to study the kynurenine pathway metabolites to understand their involvements in the development and maintenance of the inflammatory processes triggered by infections. Among them, the parasitic infection Neospora caninum could be used as a relevant model to study the role of the kynurenine pathway in the neuroinflammatory response and the subset of cells involved.

Original languageEnglish
Article number714248
Pages (from-to)1-7
Number of pages7
JournalFrontiers in Immunology
Volume12
DOIs
Publication statusPublished - 26 Jan 2022

Bibliographical note

Copyright the Author(s) 2022. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • glia
  • kynurenic acid
  • Neospora caninum
  • neuroinflammation
  • quinolinic acid

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