Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.

Superoxide radicals and other reactive oxygen species (ROS) are implicated in influenza A virus-induced inflammation. In this in vitro study, we evaluated the effects of TG6-44, a novel quinazolin-derived myeloperoxidase-specific ROS inhibitor, on influenza A virus (A/X31) infection using THP-1 lung...

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Autores principales:	Juan A De La Cruz, Thota Ganesh, Becky A Diebold, Weiping Cao, Amelia Hofstetter, Neetu Singh, Amrita Kumar, James McCoy, Priya Ranjan, Susan M E Smith, Suryaprakash Sambhara, J David Lambeth, Shivaprakash Gangappa
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/80b3ccda96934ff1811aa0a4c2c44104
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spelling	oai:doaj.org-article:80b3ccda96934ff1811aa0a4c2c441042021-12-02T20:06:51ZQuinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.1932-620310.1371/journal.pone.0254632https://doaj.org/article/80b3ccda96934ff1811aa0a4c2c441042021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0254632https://doaj.org/toc/1932-6203Superoxide radicals and other reactive oxygen species (ROS) are implicated in influenza A virus-induced inflammation. In this in vitro study, we evaluated the effects of TG6-44, a novel quinazolin-derived myeloperoxidase-specific ROS inhibitor, on influenza A virus (A/X31) infection using THP-1 lung monocytic cells and freshly isolated peripheral blood mononuclear cells (PBMC). TG6-44 significantly decreased A/X31-induced ROS and virus-induced inflammatory mediators in THP-1 cells (IL-6, IFN-γ, MCP-1, TNF-α, MIP-1β) and in human PBMC (IL-6, IL-8, TNF-α, MCP-1). Interestingly, TG6-44-treated THP-1 cells showed a decrease in percent cells expressing viral nucleoprotein, as well as a delay in translocation of viral nucleoprotein into the nucleus. Furthermore, in influenza A virus-infected cells, TG6-44 treatment led to suppression of virus-induced cell death as evidenced by decreased caspase-3 activation, decreased proportion of Annexin V+PI+ cells, and increased Bcl-2 phosphorylation. Taken together, our results demonstrate the anti-inflammatory and anti-infective effects of TG6-44.Juan A De La CruzThota GaneshBecky A DieboldWeiping CaoAmelia HofstetterNeetu SinghAmrita KumarJames McCoyPriya RanjanSusan M E SmithSuryaprakash SambharaJ David LambethShivaprakash GangappaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 7, p e0254632 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Juan A De La Cruz Thota Ganesh Becky A Diebold Weiping Cao Amelia Hofstetter Neetu Singh Amrita Kumar James McCoy Priya Ranjan Susan M E Smith Suryaprakash Sambhara J David Lambeth Shivaprakash Gangappa Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
description	Superoxide radicals and other reactive oxygen species (ROS) are implicated in influenza A virus-induced inflammation. In this in vitro study, we evaluated the effects of TG6-44, a novel quinazolin-derived myeloperoxidase-specific ROS inhibitor, on influenza A virus (A/X31) infection using THP-1 lung monocytic cells and freshly isolated peripheral blood mononuclear cells (PBMC). TG6-44 significantly decreased A/X31-induced ROS and virus-induced inflammatory mediators in THP-1 cells (IL-6, IFN-γ, MCP-1, TNF-α, MIP-1β) and in human PBMC (IL-6, IL-8, TNF-α, MCP-1). Interestingly, TG6-44-treated THP-1 cells showed a decrease in percent cells expressing viral nucleoprotein, as well as a delay in translocation of viral nucleoprotein into the nucleus. Furthermore, in influenza A virus-infected cells, TG6-44 treatment led to suppression of virus-induced cell death as evidenced by decreased caspase-3 activation, decreased proportion of Annexin V+PI+ cells, and increased Bcl-2 phosphorylation. Taken together, our results demonstrate the anti-inflammatory and anti-infective effects of TG6-44.
format	article
author	Juan A De La Cruz Thota Ganesh Becky A Diebold Weiping Cao Amelia Hofstetter Neetu Singh Amrita Kumar James McCoy Priya Ranjan Susan M E Smith Suryaprakash Sambhara J David Lambeth Shivaprakash Gangappa
author_facet	Juan A De La Cruz Thota Ganesh Becky A Diebold Weiping Cao Amelia Hofstetter Neetu Singh Amrita Kumar James McCoy Priya Ranjan Susan M E Smith Suryaprakash Sambhara J David Lambeth Shivaprakash Gangappa
author_sort	Juan A De La Cruz
title	Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
title_short	Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
title_full	Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
title_fullStr	Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
title_full_unstemmed	Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
title_sort	quinazolin-derived myeloperoxidase inhibitor suppresses influenza a virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/80b3ccda96934ff1811aa0a4c2c44104
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Quinazolin-derived myeloperoxidase inhibitor suppresses influenza A virus-induced reactive oxygen species, pro-inflammatory mediators and improves cell survival.

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