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Article ; Online: Influenza A virus M2 protein triggers mitochondrial DNA-mediated antiviral immune responses

Miyu Moriyama / Takumi Koshiba / Takeshi Ichinohe

Nature Communications, Vol 10, Iss 1, Pp 1-

2019 Volume 14

Abstract: Cytosolic mitochondrial DNA (mtDNA) plays a role in innate antiviral immunity but how this is triggered during infection remains unclear. Here, the authors provide evidence that the Influenza virus protein M2 stimulates translocation of mtDNA into the ... ...

Abstract	Cytosolic mitochondrial DNA (mtDNA) plays a role in innate antiviral immunity but how this is triggered during infection remains unclear. Here, the authors provide evidence that the Influenza virus protein M2 stimulates translocation of mtDNA into the cytosol in a MAVS-dependent manner.
Keywords	Science ; Q
Language	English
Publishing date	2019-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Influenza A virus M2 protein triggers mitochondrial DNA-mediated antiviral immune responses

Miyu Moriyama / Takumi Koshiba / Takeshi Ichinohe

Nature Communications, Vol 10, Iss 1, Pp 1-

2019 Volume 14

Abstract	Cytosolic mitochondrial DNA (mtDNA) plays a role in innate antiviral immunity but how this is triggered during infection remains unclear. Here, the authors provide evidence that the Influenza virus protein M2 stimulates translocation of mtDNA into the cytosol in a MAVS-dependent manner.
Keywords	Science ; Q
Language	English
Publishing date	2019-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Influenza Virus-Induced Oxidized DNA Activates Inflammasomes

Miyu Moriyama / Minami Nagai / Yuhei Maruzuru / Takumi Koshiba / Yasushi Kawaguchi / Takeshi Ichinohe

iScience, Vol 23, Iss 7, Pp 101270- (2020)

2020

Abstract: Summary: Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species ( ... ...

Abstract	Summary: Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species (ROS) production. However, the precise mechanism by which these viral proteins trigger the NLRP3 inflammasome activation remains unclear. Here we show that influenza virus stimulates oxidized DNA release from macrophages. Ion channel activity of the M2 protein or mitochondrial localization of the PB1-F2 protein was required for oxidized DNA release. The oxidized DNA enhanced influenza virus-induced IL-1β secretion, whereas inhibition of mitochondrial ROS production by antioxidant Mito-TEMPO decreased the virus-induced IL-1β secretion. In addition, we show that influenza virus stimulates IL-1β secretion from macrophages in an AIM2-dependent manner. These results provide a missing link between influenza viral proteins and the NLRP3 inflammasome activation and reveal the importance of influenza virus-induced oxidized DNA in inflammasomes activation.
Keywords	Immunology ; Viral Microbiology ; Science ; Q
Language	English
Publishing date	2020-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High body temperature increases gut microbiota-dependent host resistance to influenza A virus and SARS-CoV-2 infection

Minami Nagai / Miyu Moriyama / Chiharu Ishii / Hirotake Mori / Hikaru Watanabe / Taku Nakahara / Takuji Yamada / Dai Ishikawa / Takamasa Ishikawa / Akiyoshi Hirayama / Ikuo Kimura / Akihito Nagahara / Toshio Naito / Shinji Fukuda / Takeshi Ichinohe

Nature Communications, Vol 14, Iss 1, Pp 1-

2023 Volume 13

Abstract: Abstract Fever is a common symptom of influenza and coronavirus disease 2019 (COVID-19), yet its physiological role in host resistance to viral infection remains less clear. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 ...

Abstract	Abstract Fever is a common symptom of influenza and coronavirus disease 2019 (COVID-19), yet its physiological role in host resistance to viral infection remains less clear. Here, we demonstrate that exposure of mice to the high ambient temperature of 36 °C increases host resistance to viral pathogens including influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). High heat-exposed mice increase basal body temperature over 38 °C to enable more bile acids production in a gut microbiota-dependent manner. The gut microbiota-derived deoxycholic acid (DCA) and its plasma membrane-bound receptor Takeda G-protein-coupled receptor 5 (TGR5) signaling increase host resistance to influenza virus infection by suppressing virus replication and neutrophil-dependent tissue damage. Furthermore, the DCA and its nuclear farnesoid X receptor (FXR) agonist protect Syrian hamsters from lethal SARS-CoV-2 infection. Moreover, we demonstrate that certain bile acids are reduced in the plasma of COVID-19 patients who develop moderate I/II disease compared with the minor severity of illness group. These findings implicate a mechanism by which virus-induced high fever increases host resistance to influenza virus and SARS-CoV-2 in a gut microbiota-dependent manner.
Keywords	Science ; Q
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Response of host inflammasomes to viral infection

Chen, I-Yin / Takeshi Ichinohe

Trends in microbiology. 2015 Jan., v. 23, no. 1

2015

Abstract: Inflammasomes are multiprotein complexes that induce downstream immune responses to specific pathogens, environmental stimuli, and host cell damage. Components of specific viruses activate different inflammasomes; for example, the influenza A virus M2 ... ...

Abstract	Inflammasomes are multiprotein complexes that induce downstream immune responses to specific pathogens, environmental stimuli, and host cell damage. Components of specific viruses activate different inflammasomes; for example, the influenza A virus M2 protein and encephalomyocarditis virus (EMCV) 2B protein activate the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome, whereas viral double-stranded RNA (dsRNA) activates the retinoic acid inducible gene-I (RIG-I) inflammasome. Once activated in response to viral infection, inflammasomes induce the activation of caspases and the release of mature forms of interleukin-1β (IL-1β) and IL-18. Here we review the association between viral infection and inflammasome activation. Identifying the mechanisms underlying virus-induced inflammasome activation is important if we are to develop novel therapeutic strategies to target viruses.
Keywords	caspases ; double-stranded RNA ; Encephalomyocarditis virus ; immune response ; inflammasomes ; Influenza A virus ; interleukin-18 ; interleukin-1beta ; oligomerization ; pathogens ; retinoic acid ; therapeutics ; viruses
Language	English
Dates of publication	2015-01
Size	p. 55-63.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1158963-2
ISSN	1878-4380 ; 0966-842X
ISSN (online)	1878-4380
ISSN	0966-842X
DOI	10.1016/j.tim.2014.09.007
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Bonn / Germany

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Article: Induction of lung CD8+ T cell responses by consecutive inoculations of a poly(I:C) influenza vaccine

Moriyama, Miyu / Haruko Takeyama / Hideki Hasegawa / Takeshi Ichinohe

Vaccine. 2017,

2017

Abstract: The cytotoxic T lymphocyte (CTL) response plays a key role in host recovery from influenza virus infection and in subsequent immunity. Compared to natural infection with influenza virus, however, intranasal vaccination with adjuvant-combined inactivated ... ...

Abstract	The cytotoxic T lymphocyte (CTL) response plays a key role in host recovery from influenza virus infection and in subsequent immunity. Compared to natural infection with influenza virus, however, intranasal vaccination with adjuvant-combined inactivated vaccine elicits only moderate CTL responses. Here we demonstrate that 5 days of consecutive, intranasal vaccination with a combination of inactivated influenza vaccine and poly(I:C) elicits a strong CTL response in the lung. Antigen-captured respiratory DCs did efficiently migrate from the lung to the mediastinal lymph node (mLN) after the 5 day series of inoculations with vaccine and poly(I:C). Importantly, formalin-inactivated whole virus vaccine and poly(I:C) adjuvant have synergic effects on consecutive vaccinations to elicit a strong CTL response in the lung. Although the CTL response was less effective against heterologous influenza virus, we show for the first time that intranasal administration of inactivated influenza virus vaccine and poly(I:C) for 5 consecutive days can elicit high levels of influenza virus-specific CD8+ T cells in the lung.
Keywords	CD8-positive T-lymphocytes ; Orthomyxoviridae ; adjuvants ; immunity ; influenza ; influenza vaccines ; intranasal administration ; lungs ; lymph nodes ; polyinosinic-polycytidylic acid ; synergism ; vaccination ; viruses
Language	English
Size	p. .
Publishing place	Elsevier Ltd
Document type	Article
Note	Pre-press version
ZDB-ID	605674-x
ISSN	1873-2518 ; 0264-410X
ISSN (online)	1873-2518
ISSN	0264-410X
DOI	10.1016/j.vaccine.2017.10.038
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Cologne/Königswinter

Zs.A 1930: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 458: Show issues

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Article: Consecutive inoculations of influenza virus vaccine and poly(I:C) protects mice against homologous and heterologous virus challenge

Moriyama, Miyu / Shota Chino / Takeshi Ichinohe

Vaccine. 2017 Feb. 15, v. 35, no. 7

2017

Abstract: Mucosal immunity induced through natural infection by influenza virus has potent cross-protective activity, compared to subcutaneous vaccination-induced systemic immunity. Compared to natural infection with influenza virus, however, a single intranasal ... ...

Abstract	Mucosal immunity induced through natural infection by influenza virus has potent cross-protective activity, compared to subcutaneous vaccination-induced systemic immunity. Compared to natural infection with influenza virus, however, a single intranasal vaccination with an inactivated influenza virus vaccine and poly(I:C) is not sufficient to induce primary immune response in naïve animals. The reasons for this moderate effect are not fully understood. Here, we demonstrated that intranasal vaccination with formalin-inactivated influenza virus vaccine and poly(I:C) for five consecutive days elicits high levels of virus-specific nasal IgA and serum IgG responses, while vaccination without poly(I:C) induced little response. Mice immunized with influenza virus vaccine and poly(I:C) for five consecutive days sustained high levels of virus-specific IgA in nasal wash and IgG in serum until at least 6months after vaccination. Furthermore, intranasal vaccination with influenza virus vaccine and poly(I:C) protected mice against homologous and heterologous influenza virus challenge. These results suggest that consecutive inoculations of influenza virus vaccine and poly(I:C) is an alternative method to induce primary immune responses in naïve subjects.
Keywords	blood serum ; immune response ; immunoglobulin A ; immunoglobulin G ; mice ; mucosal immunity ; nose ; Orthomyxoviridae ; vaccination ; vaccines ; viruses
Language	English
Dates of publication	2017-0215
Size	p. 1001-1007.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	605674-x
ISSN	1873-2518 ; 0264-410X
ISSN (online)	1873-2518
ISSN	0264-410X
DOI	10.1016/j.vaccine.2017.01.025
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Cologne/Königswinter

Zs.A 1930: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 458: Show issues

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Article ; Online: Encephalomyocarditis virus viroporin 2B activates NLRP3 inflammasome.

Minako Ito / Yusuke Yanagi / Takeshi Ichinohe

PLoS Pathogens, Vol 8, Iss 8, p e

2012 Volume 1002857

Abstract: Nod-like receptors (NLRs) comprise a large family of intracellular pattern- recognition receptors. Members of the NLR family assemble into large multiprotein complexes, termed the inflammasomes. The NLR family, pyrin domain-containing 3 (NLRP3) is ... ...

Abstract	Nod-like receptors (NLRs) comprise a large family of intracellular pattern- recognition receptors. Members of the NLR family assemble into large multiprotein complexes, termed the inflammasomes. The NLR family, pyrin domain-containing 3 (NLRP3) is triggered by a diverse set of molecules and signals, and forms the NLRP3 inflammasome. Recent studies have indicated that both DNA and RNA viruses stimulate the NLRP3 inflammasome, leading to the secretion of interleukin 1 beta (IL-1β) and IL-18 following the activation of caspase-1. We previously demonstrated that the proton-selective ion channel M2 protein of influenza virus activates the NLRP3 inflammasome. However, the precise mechanism by which NLRP3 recognizes viral infections remains to be defined. Here, we demonstrate that encephalomyocarditis virus (EMCV), a positive strand RNA virus of the family Picornaviridae, activates the NLRP3 inflammasome in mouse dendritic cells and macrophages. Although transfection with RNA from EMCV virions or EMCV-infected cells induced robust expression of type I interferons in macrophages, it failed to stimulate secretion of IL-1β. Instead, the EMCV viroporin 2B was sufficient to cause inflammasome activation in lipopolysaccharide-primed macrophages. While cells untransfected or transfected with the gene encoding the EMCV non-structural protein 2A or 2C expressed NLRP3 uniformly throughout the cytoplasm, NLRP3 was redistributed to the perinuclear space in cells transfected with the gene encoding the EMCV 2B or influenza virus M2 protein. 2B proteins of other picornaviruses, poliovirus and enterovirus 71, also caused the NLRP3 redistribution. Elevation of the intracellular Ca(2+) level, but not mitochondrial reactive oxygen species and lysosomal cathepsin B, was important in EMCV-induced NLRP3 inflammasome activation. Chelation of extracellular Ca(2+) did not reduce virus-induced IL-1β secretion. These results indicate that EMCV activates the NLRP3 inflammasome by stimulating Ca(2+) flux from intracellular storages to the cytosol, ...
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Chlamydia pneumoniae exploits adipocyte lipid chaperone FABP4 to facilitate fat mobilization and intracellular growth in murine adipocytes

Walenna, Nirwana Fitriani / Akinori Shimizu / Bin Chou / Kazunari Ishii / Kenji Hiromatsu / Ryota Itoh / Takeshi Ichinohe / Toshinori Soejima / Yusuke Kurihara

Biochemical and biophysical research communications. 2018 Jan. 01, v. 495, no. 1

2018

Abstract: Fatty acid-binding protein 4 (FABP4), a cytosolic lipid chaperone predominantly expressed in adipocytes and macrophages, modulates lipid fluxes, trafficking, signaling, and metabolism. Recent studies have demonstrated that FABP4 regulates metabolic and ... ...

Abstract	Fatty acid-binding protein 4 (FABP4), a cytosolic lipid chaperone predominantly expressed in adipocytes and macrophages, modulates lipid fluxes, trafficking, signaling, and metabolism. Recent studies have demonstrated that FABP4 regulates metabolic and inflammatory pathways, and in mouse models its inhibition can improve type 2 diabetes mellitus and atherosclerosis. However, the role of FABP4 in bacterial infection, metabolic crosstalk between host and pathogen, and bacterial pathogenesis have not been studied. As an obligate intracellular pathogen, Chlamydia pneumoniae needs to obtain nutrients such as ATP and lipids from host cells. Here, we show that C. pneumoniae successfully infects and proliferates in murine adipocytes by inducing hormone sensitive lipase (HSL)-mediated lipolysis. Chemical inhibition or genetic manipulation of HSL significantly abrogated the intracellular growth of C. pneumoniae in adipocytes. Liberated free fatty acids were utilized to generate ATP via β-oxidation, which C. pneumoniae usurped for its replication. Strikingly, chemical inhibition or genetic silencing of FABP4 significantly abrogated C. pneumoniae infection-induced lipolysis and mobilization of liberated FFAs, resulting in reduced bacterial growth in adipocytes. Collectively, these results demonstrate that C. pneumoniae exploits host FABP4 to facilitate fat mobilization and intracellular replication in adipocytes. This work uncovers a novel strategy used by intracellular pathogens for acquiring energy via hijacking of the host lipid metabolism pathway.
Keywords	adenosine triphosphate ; adipocytes ; animal models ; atherosclerosis ; bacterial infections ; beta oxidation ; carboxylic ester hydrolases ; Chlamydophila pneumoniae ; energy ; fatty acid-binding proteins ; free fatty acids ; genetic engineering ; lipids ; lipolysis ; macrophages ; mice ; microbial growth ; nutrients ; pathogenesis ; pathogens
Language	English
Dates of publication	2018-0101
Size	p. 353-359.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2017.11.005
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: TLR7 mediated viral recognition results in focal type I interferon secretion by dendritic cells

Shin-Ichiroh Saitoh / Fumiko Abe / Atsuo Kanno / Natsuko Tanimura / Yoshiko Mori Saitoh / Ryutaro Fukui / Takuma Shibata / Katsuaki Sato / Takeshi Ichinohe / Mayumi Hayashi / Kazuishi Kubota / Hiroko Kozuka-Hata / Masaaki Oyama / Yorifumi Kikko / Toshiaki Katada / Kenji Kontani / Kensuke Miyake

Nature Communications, Vol 8, Iss 1, Pp 1-

2017 Volume 12

Abstract: Antiviral immune responses involve clustering of plasmacytoid dendritic cells (pDC) in response to endosomal TLR7-mediated sensing of viral RNA. Here the authors show the GTPase Arl8b controls translocation of TLR7+ endosomes to the periphery of the cell ...

Abstract	Antiviral immune responses involve clustering of plasmacytoid dendritic cells (pDC) in response to endosomal TLR7-mediated sensing of viral RNA. Here the authors show the GTPase Arl8b controls translocation of TLR7+ endosomes to the periphery of the cell via microtubule interactions, thus enabling pDC clustering and type I interferon production.
Keywords	Science ; Q
Language	English
Publishing date	2017-11-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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