Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury

Abstract One of the hallmarks of acute inflammation is neutrophil infiltration of tissues. We investigated molecular mechanisms implicated in acute neutrophilic inflammation induced by the venom of a freshwater stingray (Potamotrygon cf. henlei) in mice. Ray venom induced early mobilization of neutr...

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Autores principales:	Janaina Cardoso dos Santos, Lidiane Zito Grund, Carla Simone Seibert, Elineide Eugênio Marques, Anderson Brito Soares, Valerie F. Quesniaux, Bernhard Ryffel, Monica Lopes-Ferreira, Carla Lima
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a71029b927c446c9877ba62f7121f0f1
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spelling	oai:doaj.org-article:a71029b927c446c9877ba62f7121f0f12021-12-02T16:06:15ZStingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury10.1038/s41598-017-08395-y2045-2322https://doaj.org/article/a71029b927c446c9877ba62f7121f0f12017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08395-yhttps://doaj.org/toc/2045-2322Abstract One of the hallmarks of acute inflammation is neutrophil infiltration of tissues. We investigated molecular mechanisms implicated in acute neutrophilic inflammation induced by the venom of a freshwater stingray (Potamotrygon cf. henlei) in mice. Ray venom induced early mobilization of neutrophil in the microvasculature of cremaster mice and infiltration of the peritoneal cavity 2 hours after injury, in a dose-response manner. IL-1β, IL-6, TNF-α, and KC were produced. The neutrophilic infiltration did not occur in mice with ST2 receptor and MyD88 adapters neutralized, or in those with PI3K and p38 MAPK signaling blocked. Drastic reduction of neutrophil infiltration to peritoneal cavities was observed in ST2−/−, TLR2/TLR4−/−, MyD88−/−, TRIF−/− and IL-17A−/− mice, and a partial reduction was observed in IL-18R−/− mice. Mast cell Kit W(sh)/W(sh)-, AHR-, NLRP3-, ICE-, IL-1β-, P2RX7-, CD39-, IL-17RA-, and TBX21 KO mice retain the ability to induce neutrophilia in peritoneal cavity after ray venom injection. IL-6 and TNF-α alone were insufficient for promote neutrophilia in the absence of ST2 signaling. Finally, abundant production of IL-33 by cardiomyocytes was observed. These results refine our understanding of the importance of the IL-33/ST2 axis and IL-33-producing cardiomyocytes in the early acute neutrophilia induced by freshwater stingray venoms.Janaina Cardoso dos SantosLidiane Zito GrundCarla Simone SeibertElineide Eugênio MarquesAnderson Brito SoaresValerie F. QuesniauxBernhard RyffelMonica Lopes-FerreiraCarla LimaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Janaina Cardoso dos Santos Lidiane Zito Grund Carla Simone Seibert Elineide Eugênio Marques Anderson Brito Soares Valerie F. Quesniaux Bernhard Ryffel Monica Lopes-Ferreira Carla Lima Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
description	Abstract One of the hallmarks of acute inflammation is neutrophil infiltration of tissues. We investigated molecular mechanisms implicated in acute neutrophilic inflammation induced by the venom of a freshwater stingray (Potamotrygon cf. henlei) in mice. Ray venom induced early mobilization of neutrophil in the microvasculature of cremaster mice and infiltration of the peritoneal cavity 2 hours after injury, in a dose-response manner. IL-1β, IL-6, TNF-α, and KC were produced. The neutrophilic infiltration did not occur in mice with ST2 receptor and MyD88 adapters neutralized, or in those with PI3K and p38 MAPK signaling blocked. Drastic reduction of neutrophil infiltration to peritoneal cavities was observed in ST2−/−, TLR2/TLR4−/−, MyD88−/−, TRIF−/− and IL-17A−/− mice, and a partial reduction was observed in IL-18R−/− mice. Mast cell Kit W(sh)/W(sh)-, AHR-, NLRP3-, ICE-, IL-1β-, P2RX7-, CD39-, IL-17RA-, and TBX21 KO mice retain the ability to induce neutrophilia in peritoneal cavity after ray venom injection. IL-6 and TNF-α alone were insufficient for promote neutrophilia in the absence of ST2 signaling. Finally, abundant production of IL-33 by cardiomyocytes was observed. These results refine our understanding of the importance of the IL-33/ST2 axis and IL-33-producing cardiomyocytes in the early acute neutrophilia induced by freshwater stingray venoms.
format	article
author	Janaina Cardoso dos Santos Lidiane Zito Grund Carla Simone Seibert Elineide Eugênio Marques Anderson Brito Soares Valerie F. Quesniaux Bernhard Ryffel Monica Lopes-Ferreira Carla Lima
author_facet	Janaina Cardoso dos Santos Lidiane Zito Grund Carla Simone Seibert Elineide Eugênio Marques Anderson Brito Soares Valerie F. Quesniaux Bernhard Ryffel Monica Lopes-Ferreira Carla Lima
author_sort	Janaina Cardoso dos Santos
title	Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
title_short	Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
title_full	Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
title_fullStr	Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
title_full_unstemmed	Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
title_sort	stingray venom activates il-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/a71029b927c446c9877ba62f7121f0f1
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Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury

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