Interleukin-1 receptor-induced PGE2 production controls acetylcholine-mediated cardiac dysfunction and mortality during scorpion envenomation

Mouzarllem B. Reis, Fernanda L. Rodrigues, Natalia Lautherbach, Alexandre Kanashiro, Carlos A. Sorgi, Alyne F. G. Meirelles, Carlos A. A. Silva, Karina F. Zoccal, Camila O. S. Souza, Simone G. Ramos, Alessandra K. Matsuno, Lenaldo B. Rocha, Helio C. Salgado, Luiz C. C. Navegantes, Ísis C. Kettelhut, Palmira Cupo, Luiz G. Gardinassi and Lúcia H. Faccioli ()
Additional contact information
Mouzarllem B. Reis: Universidade de São Paulo
Fernanda L. Rodrigues: Universidade de São Paulo
Natalia Lautherbach: Universidade de São Paulo
Alexandre Kanashiro: Universidade de São Paulo
Carlos A. Sorgi: Universidade de São Paulo
Alyne F. G. Meirelles: Universidade de São Paulo
Carlos A. A. Silva: Universidade de São Paulo
Karina F. Zoccal: Centro Universitário Barão de Mauá
Camila O. S. Souza: Universidade de São Paulo
Simone G. Ramos: Faculdade de Medicina de Ribeirão Preto
Alessandra K. Matsuno: Faculdade de Medicina de Ribeirão Preto
Lenaldo B. Rocha: Universidade Federal do Triângulo Mineiro
Helio C. Salgado: Universidade de São Paulo
Luiz C. C. Navegantes: Universidade de São Paulo
Ísis C. Kettelhut: Universidade de São Paulo
Palmira Cupo: Faculdade de Medicina de Ribeirão Preto
Luiz G. Gardinassi: Universidade de São Paulo
Lúcia H. Faccioli: Universidade de São Paulo

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Scorpion envenomation is a leading cause of morbidity and mortality among accidents caused by venomous animals. Major clinical manifestations that precede death after scorpion envenomation include heart failure and pulmonary edema. Here, we demonstrate that cardiac dysfunction and fatal outcomes caused by lethal scorpion envenomation in mice are mediated by a neuro-immune interaction linking IL-1 receptor signaling, prostaglandin E2, and acetylcholine release. IL-1R deficiency, the treatment with a high dose of dexamethasone or blockage of parasympathetic signaling using atropine or vagotomy, abolished heart failure and mortality of envenomed mice. Therefore, we propose the use of dexamethasone administration very early after envenomation, even before antiserum, to inhibit the production of inflammatory mediators and acetylcholine release, and to reduce the risk of death.

Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19232-8

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DOI: 10.1038/s41467-020-19232-8

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