Authors
Livia Claude, Frédéric Martino, Lydiane Mordier, Doris Célanie, Emmanuelle Bernit, Maryse Etienne-Julan, Benoît Tressières, Marc Romana, Véronique Baccini
Published in
Journal of cellular and molecular medicine. Volume 30. Issue 20. Pages e71390.
Abstract
Sickle cell disease (SCD) is characterized by hemolytic anaemia, painful vaso-occlusive crises, and chronic inflammation resulting partly from platelet activation. It has been shown that platelets express the nucleotide-binding domain leucine-rich repeat containing protein 3 (NLRP3) and the apoptosis-associated speck-like protein containing a CARD (ASC), forming the NLRP3 inflammasome, which controls activation of caspase-1 and cleavage of interleukin-1β (IL-1β). Bruton tyrosine kinase (BTK), known to activate the NLRP3 inflammasome, is also expressed in platelets. In SCD, platelets are activated and can secrete increased quantities of IL-1β, suggesting a possible activation of the NLRP3 inflammasome. Here, we assessed platelet P-selectin expression, caspase-1 activation, platelet-neutrophil aggregate formations by flow cytometry and BTK phosphorylation by Western blot in a cohort of 81 adult SCD patients at steady state condition (34 SC and 47 SS patients). We showed an increase in platelet activation in sickle patients and a high level of platelet-neutrophil aggregate in SS patients compared to healthy subjects (17 AA). We also demonstrated platelet caspase-1 activation in SCD patients and obtained data suggesting for the first time NLRP3 inflammasome activation in SC patients. Further studies are needed to understand the mechanism of caspase-1 activation and evaluate the potential therapeutic efficiency of Ibrutinib, a BTK inhibitor.
PMID:
42875993
Bibliographic data and abstract were imported from PubMed on 15 Oct 2026.
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