ROLE OF PGE2 ON NEUTROPHILS DURING HUMAN TUBERCULO

CANDELA MARTIN; NANCY TATEOSIAN; DOMINGO J. PALMERO; MARÍA PAULA MORELLI; LORENA CIALLELLA; JOAQUIN M. PELLEGRINI; NICOLÁS O. AMIANO; VERÓNICA E. GARCIA

Simposio; Tuberculosis: Science Aimed at Ending the Epidemic; 2020

Keystone Symposia

Tuberculosis (TB) is one of the top 10 causes of death worldwide. Prostaglandin E2 (PGE2), an active lipid compound derived from arachidonic acid, regulates different stages of the response of the host during several pathologies such as chronic infections or cancer. Interestingly, manipulation of PGE2 levels was proposed as an approach for countering the Type I IFN signature of TB 1, although very limited information about this pathway in tuberculosis patients is available. Therefore, the aim of the present work was to investigate the role of this compound during human TB. Neutrophils were obtained from heparinized peripheral blood from healthy donors (HD) and tuberculosis patients (TB) by Ficoll-Hypaque centrifugation and Dextran sedimentation. Cells were cultured with a Mycobacterium tuberculosis lysate (Mtb-Ag, 10μg/ml) with/without PGE2. Then, we evaluated the role of this lipidic mediator during the human immune response against Mtb-Ag by using flow cytometry and confocal microscopy assays. P-values