PB0749 - Platelet reactivity with Plasmodium vivax proteins

Monday, June 26, 2023

18:30 – 19:30 ET

Room: Exhibition

Co-Author(s)

PG

Patricia Guzman-Cancino, MsC

Master' student
Universidad Michoacana de San Nicolás de Hidalgo
Morelia, Michoacan de Ocampo, Mexico

Co-Author(s)

NG

Nallely I. García-Larragoiti

Posdoc Research
Facultad de Ciencias Medicas y Biológicas "Dr. Ignacio Chávez". Universidad Michoacana de San Nicolás de Hidalgo
Morelia, Michoacan de Ocampo, Mexico

Presenting Author(s)

Alan Cano Méndez, PhD (he/him/his)

Facultad de Ciencias Medicas y Biológicas "Dr. Ignacio Chávez". Universidad Michoacana de San Nicolás de Hidalgo
Morelia, Michoacan de Ocampo, Mexico

Co-Author(s)

MD

Maria Guadalupe Damian-Vazquez

Master in science
Universidad Michoacana de San Nicolás de Hidalgo
Morelia, Michoacan de Ocampo, Mexico
YJ

Yeny Jiménez-Vega

PREGRADE STUDENT
MICHOACAN UNIVERSITY OF SAN NICOLAS DE HIDALGO
MORELIA, Michoacan de Ocampo, Mexico
MT

Mercedes Trujillo

PREGRADE STUDENT
MICHOACAN UNIVERSITY OF SAN NICOLAS DE HIDALGO
MORELIA, Michoacan de Ocampo, Mexico
AR

Arturo Reyes-Sandoval

PhD
Instituto Politecnico Nacional
Ciudad de México, Distrito Federal, Mexico
MV

Martha Eva Viveros-Sandoval

Professor
Facultad de Ciencias Medicas y Biológicas "Dr. Ignacio Chávez". Universidad Michoacana de San Nicolás de Hidalgo
Morelia, Michoacan de Ocampo, Mexico

Background: Plasmodium vivax is responsible for malaria cases in America. The sporozoites travel through bloodstream to the liver and carry out a pre-erythrocyte infection where it uses specific proteins such as PvTRAP and CSP responsible for parasite motility. Once the infection is established, these parasites use CelTOS protein to leave the hepatocyte and carry out an erythrocyte infection that causes damage to endothelial cells promoting activation of procoagulant and inflammatory processes, leading to platelet activation causing thrombocytopenia, aggravating the disease which can cause death. There is no information on the platelet response to CelTOS, PvTRAP and CSP proteins.

Aims: Study platelet reactivity to Plasmodium vivax CelTOS, PvTRAP, and CSP proteins.

Methods: Blood samples were obtained from healthy volunteers by venipuncture, using 3.2% sodium citrate as an anticoagulant. Platelet-rich plasma (PRP) was obtained by slow centrifugation (1000 rpm x 10 minutes). PRP was isolated and resuspended in Tyrodes buffer. PRP was incubated for 1 hour with Plasmodium vivax PvTRAP, CelTOS, and CSP proteins (kindly provided by Arturo Reyes Laboratory, Jenner Institute, Oxford University) in individual assays. Platelet activity was assessed by flow cytometry: CD41-PECy7, CD62-PE, and PAC1-FITC. We evaluated the ability of proteins to induce platelet aggregation by aggregometry. ADP 20µM, collagen 20 Um, and epinephrine 100µM were used as known platelet activation agonists.

Results: We observed platelet reactivity after stimulation with PvTRAP, CelTOS, and CSP proteins similar to that observed with known activation agonists. None of the proteins were able to induce platelet aggregation. However, PRP treated with CSP and a minimal dose of collagen (2 uM) added was able to induce cell aggregation.

Conclusion(s): Malaria CSP, CelTOS, and PvTRAP proteins induce platelet reactivity.