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Peer-reviewedCC BYJournal of cellular and molecular medicine

Activation of Platelet Caspase-1 and P-Selectin Over-Expression in Sickle Cell Disease Patients: An Involvement of NLRP3 Inflammasome?

  • Livia Claude1,2
  • Frédéric Martino1,3
  • Lydiane Mordier1
  • Doris Célanie1
  • Emmanuelle Bernit4
  • Maryse Etienne-Julan1,4
  • Benoît Tressières5
  • Marc Romana1
  • Véronique Baccini1,2
5 affiliations
  1. 1INSERM, BIGR, Université Paris Cité and Université des Antilles, Paris, France.
  2. 2Laboratoire d'Hématologie, CHU de la Guadeloupe, Pointe-à-Pitre, Guadeloupe.
  3. 3Service de Réanimation, CHU de la Guadeloupe, Pointe-à-Pitre, Guadeloupe.
  4. 4Unité Transversale de la Drépanocytose, CHU de la Guadeloupe, Hôpital Ricou, Pointe-à-Pitre, Guadeloupe.
  5. 5Centre d'Investigation Clinique Antilles Guyane, Inserm CIC 1424, CHU de la Guadeloupe, Pointe-à-Pitre, Guadeloupe.
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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.

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Cite

BibTeXRIS
BibTeX
@article{claude2026activation,
  title = {{Activation of Platelet Caspase-1 and P-Selectin Over-Expression in Sickle Cell Disease Patients: An Involvement of NLRP3 Inflammasome?}},
  author = {Livia Claude and Frédéric Martino and Lydiane Mordier and Doris Célanie and Emmanuelle Bernit and Maryse Etienne-Julan and Benoît Tressières and Marc Romana and Véronique Baccini},
  journal = {Journal of cellular and molecular medicine},
  year = {2026},
  month = oct,
  doi = {10.1111/jcmm.71390},
  url = {https://europepmc.org/article/MED/42875993},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Activation of Platelet Caspase-1 and P-Selectin Over-Expression in Sickle Cell Disease Patients: An Involvement of NLRP3 Inflammasome?
AU  - Livia Claude
AU  - Frédéric Martino
AU  - Lydiane Mordier
AU  - Doris Célanie
AU  - Emmanuelle Bernit
AU  - Maryse Etienne-Julan
AU  - Benoît Tressières
AU  - Marc Romana
AU  - Véronique Baccini
PY  - 2026
DA  - 2026/10/01
JO  - Journal of cellular and molecular medicine
DO  - 10.1111/jcmm.71390
UR  - https://europepmc.org/article/MED/42875993
AB  - 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.
SN  - 1582-1838
SN  - 1582-4934
ER  -