CD300a contributes to the resolution of articular inflammation triggered by MSU crystals by controlling neutrophil apoptosis

Bruno V.S. Valiate*, Celso M. Queiroz-Junior, Francesca Levi-Schaffer, Izabela Galvão, Mauro M. Teixeira

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Gout is an inflammatory disease triggered by deposition of monosodium urate (MSU) crystals in the joints, resulting in high neutrophil influx and pain. Here, we studied the role of the inhibitory receptor CD300a in the resolution process in a murine model of gout. We found increased CD300a expression on neutrophils emigrated to the joint. When compared to WT mice, CD300a−/− mice had persistent neutrophil influx till 24 hr after MSU injection. This was associated with increased concentration of IL-1β and greater tissue damage in the joints of CD300a−/− mice. There was an increase in the percentage of apoptotic neutrophils in the synovial lavage of WT mice, as compared to CD300a−/− mice. This difference was reflected in the decline of efferocytic events in the synovial cavity of CD300a−/− mice 24 hr after MSU injection. A CD300a agonistic antibody was shown, for the first time, to increase apoptosis of human neutrophils, and this was associated with cleavage of caspase-8. In conclusion, our results reveal an important role of CD300a in the control of leucocyte infiltration, IL-1β production and caspase-8 cleavage in neutrophils, contributing to the resolution of inflammation triggered by MSU injection.

Original languageAmerican English
Pages (from-to)305-317
Number of pages13
JournalImmunology
Volume164
Issue number2
DOIs
StatePublished - Oct 2021

Bibliographical note

Publisher Copyright:
© 2021 John Wiley & Sons Ltd.

Keywords

  • CD300a
  • apoptosis
  • gout
  • neutrophilic inflammation
  • resolution of inflammation

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