A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice

Abstract Molecular mimicry is one of the main processes for producing autoantibodies during infections. Although some autoantibodies are associated with autoimmune diseases, the functions of many autoantibodies remain unknown. Previously, we reported that S16, a mouse (BALB/c) monoclonal antibody ag...

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Autores principales:	Yutaka Sasaki, Naoto Yoshino, Takako Okuwa, Takashi Odagiri, Takashi Satoh, Yasushi Muraki
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/687ec43af0d341c7ac7746c8d4f5fb3d
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spelling	oai:doaj.org-article:687ec43af0d341c7ac7746c8d4f5fb3d2021-12-02T18:24:54ZA mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice10.1038/s41598-021-91251-x2045-2322https://doaj.org/article/687ec43af0d341c7ac7746c8d4f5fb3d2021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-91251-xhttps://doaj.org/toc/2045-2322Abstract Molecular mimicry is one of the main processes for producing autoantibodies during infections. Although some autoantibodies are associated with autoimmune diseases, the functions of many autoantibodies remain unknown. Previously, we reported that S16, a mouse (BALB/c) monoclonal antibody against the hemagglutinin-esterase fusion glycoprotein of influenza C virus, recognizes host proteins in some species of animals, but we could not succeed in identifying the proteins. In the present study, we found that S16 cross-reacted with acetyl-CoA acyltransferase 2 (ACAA2), which is expressed in the livers of BALB/c mice. ACAA2 was released into the serum after acetaminophen (APAP) administration, and its serum level correlated with serum alanine aminotransferase (ALT) activity. Furthermore, we observed that S16 injected into mice with APAP-induced hepatic injury prompted the formation of an immune complex between S16 and ACAA2 in the serum. The levels of serum ALT (p < 0.01) and necrotic areas in the liver (p < 0.01) were reduced in the S16-injected mice. These results suggest that S16 may have a mitigation function in response to APAP-induced hepatotoxicity. This study shows the therapeutic function of an autoantibody and suggests that an antibody against extracellular ACAA2 might be a candidate for treating APAP-induced hepatic injury.Yutaka SasakiNaoto YoshinoTakako OkuwaTakashi OdagiriTakashi SatohYasushi MurakiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yutaka Sasaki Naoto Yoshino Takako Okuwa Takashi Odagiri Takashi Satoh Yasushi Muraki A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice
description	Abstract Molecular mimicry is one of the main processes for producing autoantibodies during infections. Although some autoantibodies are associated with autoimmune diseases, the functions of many autoantibodies remain unknown. Previously, we reported that S16, a mouse (BALB/c) monoclonal antibody against the hemagglutinin-esterase fusion glycoprotein of influenza C virus, recognizes host proteins in some species of animals, but we could not succeed in identifying the proteins. In the present study, we found that S16 cross-reacted with acetyl-CoA acyltransferase 2 (ACAA2), which is expressed in the livers of BALB/c mice. ACAA2 was released into the serum after acetaminophen (APAP) administration, and its serum level correlated with serum alanine aminotransferase (ALT) activity. Furthermore, we observed that S16 injected into mice with APAP-induced hepatic injury prompted the formation of an immune complex between S16 and ACAA2 in the serum. The levels of serum ALT (p < 0.01) and necrotic areas in the liver (p < 0.01) were reduced in the S16-injected mice. These results suggest that S16 may have a mitigation function in response to APAP-induced hepatotoxicity. This study shows the therapeutic function of an autoantibody and suggests that an antibody against extracellular ACAA2 might be a candidate for treating APAP-induced hepatic injury.
format	article
author	Yutaka Sasaki Naoto Yoshino Takako Okuwa Takashi Odagiri Takashi Satoh Yasushi Muraki
author_facet	Yutaka Sasaki Naoto Yoshino Takako Okuwa Takashi Odagiri Takashi Satoh Yasushi Muraki
author_sort	Yutaka Sasaki
title	A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice
title_short	A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice
title_full	A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice
title_fullStr	A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice
title_full_unstemmed	A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice
title_sort	mouse monoclonal antibody against influenza c virus attenuates acetaminophen-induced liver injury in mice
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/687ec43af0d341c7ac7746c8d4f5fb3d
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A mouse monoclonal antibody against influenza C virus attenuates acetaminophen-induced liver injury in mice

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