Blockade of Caspase Cascade Overcomes Malaria-associated Acute Respiratory Distress Syndrome in Mice

Overview

Journal Cell Death Dis

Specialties Cell Biology
General Medicine

Date 2022 Feb 11

PMID 35145061

Authors

Michelle K Sercundes

Luana S Ortolan

Viviane da Silva Julio

Leonardo M Bella

Thatyane de Castro Quirino

Daniela Debone

Marcela S Carneiro-Ramos

Marcelo A Christoffolete

Joilson O Martins

Maria Regina DImperio Lima

Jose M Alvarez

Gustavo P Amarante-Mendes

Ligia Antunes Goncalves

Claudio R F Marinho

Sabrina Epiphanio

Affiliations

Soon will be listed here.

Abstract

Malaria is an enormous burden on global health that caused 409,000 deaths in 2019. Severe malaria can manifest in the lungs, an illness known as acute respiratory distress syndrome (ARDS). Not much is known about the development of malaria-associated ARDS (MA-ARDS), especially regarding cell death in the lungs. We had previously established a murine model that mimics various human ARDS aspects, such as pulmonary edema, hemorrhages, pleural effusion, and hypoxemia, using DBA/2 mice infected with Plasmodium berghei ANKA. Here, we explored the mechanisms and the involvement of apoptosis in this syndrome. We found that apoptosis contributes to the pathogenesis of MA-ARDS, primarily as facilitators of the alveolar-capillary barrier breakdown. The protection of pulmonary endothelium by inhibiting caspase activation could be a promising therapeutic strategy to prevent the pathogenicity of MA-ARDS. Therefore, intervention in the programmed death cell mechanism could help patients not to develop severe malaria.

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