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TRPV1 Contributes to Cerebral Malaria Severity and Mortality by Regulating Brain Inflammation.

Abstract：

:Transient receptor potential vanilloid 1 (TRPV1) is a Ca+2-permeable channel expressed on neuronal and nonneuronal cells, known as an oxidative stress sensor. It plays a protective role in bacterial infection, and recent findings indicate that this receptor modulates monocyte populations in mice with malaria; however, its role in cerebral malaria progression and outcome is unclear. By using TRPV1 wild-type (WT) and knockout (KO) mice, the importance of TRPV1 to this cerebral syndrome was investigated. Infection with Plasmodium berghei ANKA decreased TRPV1 expression in the brain. Mice lacking TRPV1 were protected against Plasmodium-induced mortality and morbidity, a response that was associated with less cerebral swelling, modulation of the brain expression of endothelial tight-junction markers (junctional adhesion molecule A and claudin-5), increased oxidative stress (via inhibition of catalase activity and increased levels of H2O2, nitrotyrosine, and carbonyl residues), and diminished production of cytokines. Plasmodium load was not significantly affected by TRPV1 ablation. Repeated subcutaneous administration of the selective TRPV1 antagonist SB366791 after malaria induction increased TRPV1 expression in the brain tissue and enhanced mouse survival. These data indicate that TRPV1 channels contribute to the development and outcome of cerebral malaria.

journal_name

Oxid Med Cell Longev

journal_title

Oxidative medicine and cellular longevity

authors

Pereira DMS,Teixeira SA,Murillo O,Peixoto EPM,Araújo MC,Sousa NCF,Monteiro-Neto V,Calixto JB,Cunha TM,Marinho CRF,Muscará MN,Fernandes ES

doi

10.1155/2019/9451671

subject

Has Abstract

pub_date

2019-05-16 00:00:00

pages

9451671

eissn

1942-0900

issn

1942-0994

journal_volume

2019

pub_type

杂志文章

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