Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model

Abstract Although coagulation abnormalities, including microvascular thrombosis, are thought to contribute to tissue injury and single- or multiple-organ dysfunction in severe influenza, the detailed mechanisms have yet been clarified. This study evaluated influenza-associated abnormal blood coagula...

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Autores principales:	Marumi Ohno, Akemi Kakino, Toshiki Sekiya, Naoki Nomura, Masashi Shingai, Tatsuya Sawamura, Hiroshi Kida
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7ac7521ebd7042ffafcaf8c0932031fb
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spelling	oai:doaj.org-article:7ac7521ebd7042ffafcaf8c0932031fb2021-12-02T17:06:09ZCritical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model10.1038/s41598-021-95046-y2045-2322https://doaj.org/article/7ac7521ebd7042ffafcaf8c0932031fb2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-95046-yhttps://doaj.org/toc/2045-2322Abstract Although coagulation abnormalities, including microvascular thrombosis, are thought to contribute to tissue injury and single- or multiple-organ dysfunction in severe influenza, the detailed mechanisms have yet been clarified. This study evaluated influenza-associated abnormal blood coagulation utilizing a severe influenza mouse model. After infecting C57BL/6 male mice with intranasal applications of 500 plaque-forming units of influenza virus A/Puerto Rico/8/34 (H1N1; PR8), an elevated serum level of prothrombin fragment 1 + 2, an indicator for activated thrombin generation, was observed. Also, an increased gene expression of oxidized low-density lipoprotein (LDL) receptor-1 (Olr1), a key molecule in endothelial dysfunction in the progression of atherosclerosis, was detected in the aorta of infected mice. Body weight decrease, serum levels of cytokines and chemokines, viral load, and inflammation in the lungs of infected animals were similar between wild-type and Olr1 knockout (KO) mice. In contrast, the elevation of prothrombin fragment 1 + 2 levels in the sera and intravascular thrombosis in the lungs by PR8 virus infection were not induced in KO mice. Collectively, the results indicated that OLR1 is a critical host factor in intravascular thrombosis as a pathogeny of severe influenza. Thus, OLR1 is a promising novel therapeutic target for thrombosis during severe influenza.Marumi OhnoAkemi KakinoToshiki SekiyaNaoki NomuraMasashi ShingaiTatsuya SawamuraHiroshi KidaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Marumi Ohno Akemi Kakino Toshiki Sekiya Naoki Nomura Masashi Shingai Tatsuya Sawamura Hiroshi Kida Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model
description	Abstract Although coagulation abnormalities, including microvascular thrombosis, are thought to contribute to tissue injury and single- or multiple-organ dysfunction in severe influenza, the detailed mechanisms have yet been clarified. This study evaluated influenza-associated abnormal blood coagulation utilizing a severe influenza mouse model. After infecting C57BL/6 male mice with intranasal applications of 500 plaque-forming units of influenza virus A/Puerto Rico/8/34 (H1N1; PR8), an elevated serum level of prothrombin fragment 1 + 2, an indicator for activated thrombin generation, was observed. Also, an increased gene expression of oxidized low-density lipoprotein (LDL) receptor-1 (Olr1), a key molecule in endothelial dysfunction in the progression of atherosclerosis, was detected in the aorta of infected mice. Body weight decrease, serum levels of cytokines and chemokines, viral load, and inflammation in the lungs of infected animals were similar between wild-type and Olr1 knockout (KO) mice. In contrast, the elevation of prothrombin fragment 1 + 2 levels in the sera and intravascular thrombosis in the lungs by PR8 virus infection were not induced in KO mice. Collectively, the results indicated that OLR1 is a critical host factor in intravascular thrombosis as a pathogeny of severe influenza. Thus, OLR1 is a promising novel therapeutic target for thrombosis during severe influenza.
format	article
author	Marumi Ohno Akemi Kakino Toshiki Sekiya Naoki Nomura Masashi Shingai Tatsuya Sawamura Hiroshi Kida
author_facet	Marumi Ohno Akemi Kakino Toshiki Sekiya Naoki Nomura Masashi Shingai Tatsuya Sawamura Hiroshi Kida
author_sort	Marumi Ohno
title	Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model
title_short	Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model
title_full	Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model
title_fullStr	Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model
title_full_unstemmed	Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model
title_sort	critical role of oxidized ldl receptor-1 in intravascular thrombosis in a severe influenza mouse model
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/7ac7521ebd7042ffafcaf8c0932031fb
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Critical role of oxidized LDL receptor-1 in intravascular thrombosis in a severe influenza mouse model

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