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Book ; Online ; Thesis: Analysis of the role of different pattern recognition receptors in murine cytomegalovirus-mediated activation of innate immunity

Tegtmeyer, Pia-Katharina [Verfasser] / Kalinke, Ulrich [Akademischer Betreuer] / Messerle, Martin [Akademischer Betreuer]

2019

Author's details	Pia-Katharina Tegtmeyer ; Akademische Betreuer: Ulrich Kalinke, Martin Messerle ; TWINCORE, Zentrum für Experimentelle und Klinische Infektionsforschung; Institut für Experimentelle Infektionsforschung
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	German
Publisher	Bibliothek der Medizinischen Hochschule Hannover
Publishing place	Hannover
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Corrigendum to: 'Hepatocyte-specific suppression of microRNA-221-3p mitigates liver fibrosis' [J Hepatol (2019) 722-734].

Tsay, Hsin-Chieh / Yuan, Qinggong / Balakrishnan, Asha / Kaiser, Marina / Möbus, Selina / Kozdrowska, Emilia / Farid, Marwa / Tegtmeyer, Pia-Katharina / Borst, Katharina / Vondran, Florian W R / Kalinke, Ulrich / Kispert, Andreas / Manns, Michael P / Ott, Michael / Sharma, Amar Deep

Journal of hepatology

2022 Volume 77, Issue 1, Page(s) 269

Language	English
Publishing date	2022-04-06
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.03.022
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Article ; Online: STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Tegtmeyer, Pia-Katharina / Spanier, Julia / Borst, Katharina / Becker, Jennifer / Riedl, André / Hirche, Christoph / Ghita, Luca / Skerra, Jennifer / Baumann, Kira / Lienenklaus, Stefan / Doering, Marius / Ruzsics, Zsolt / Kalinke, Ulrich

Nature communications

2019 Volume 10, Issue 1, Page(s) 2830

Abstract: Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine ... ...

Abstract	Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.
MeSH term(s)	Animals ; Female ; Hepatocytes/metabolism ; Hepatocytes/virology ; Herpesviridae Infections/veterinary ; Herpesviridae Infections/virology ; Host-Pathogen Interactions ; Interferon-beta/genetics ; Interferon-beta/metabolism ; Kupffer Cells/metabolism ; Kupffer Cells/virology ; Liver/metabolism ; Liver/virology ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muromegalovirus/genetics ; Muromegalovirus/physiology ; Myeloid Cells/metabolism ; Myeloid Cells/virology ; Rodent Diseases/genetics ; Rodent Diseases/metabolism ; Rodent Diseases/virology ; Signal Transduction ; Toll-Like Receptors/genetics ; Toll-Like Receptors/metabolism
Chemical Substances	Membrane Proteins ; Sting1 protein, mouse ; Toll-Like Receptors ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2019-06-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-10863-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Human monocyte-derived macrophages inhibit HCMV spread independent of classical antiviral cytokines.

Becker, Jennifer / Kinast, Volker / Döring, Marius / Lipps, Christoph / Duran, Veronica / Spanier, Julia / Tegtmeyer, Pia-Katharina / Wirth, Dagmar / Cicin-Sain, Luka / Alcamí, Antonio / Kalinke, Ulrich

Virulence

2018 Volume 9, Issue 1, Page(s) 1669–1684

Abstract: Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To ... ...

Abstract	Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To better understand HCMV pathogenesis we studied mechanisms that restrict HCMV spread. We discovered that HCMV-infected cells can directly trigger plasmacytoid dendritic cells (pDC) to mount antiviral type I interferon (IFN-I) responses, even in the absence of cell-free virus. In contrast, monocyte-derived cells only expressed IFN-I when stimulated by cell-free HCMV, or upon encounter of HCMV-infected cells that already produced cell-free virus. Nevertheless, also in the absence of cell-free virus, i.e., upon co-culture of infected epithelial/endothelial cells and monocyte-derived macrophages (moMΦ) or dendritic cells (moDC), antiviral responses were induced that limited HCMV spread. The induction of this antiviral effect was dependent on cell-cell contact, whereas cell-free supernatants from co-culture experiments also inhibited virus spread, implying that soluble factors were critically needed. Interestingly, the antiviral effect was independent of IFN-γ, TNF-α, and IFN-I as indicated by cytokine inhibition experiments using neutralizing antibodies or the vaccinia virus-derived soluble IFN-I binding protein B18R, which traps human IFN-α and IFN-β. In conclusion, our results indicate that human macrophages and dendritic cells can limit HCMV spread by IFN-I dependent as well as independent mechanisms, whereas the latter ones might be particularly relevant for the restriction of HCMV transmission via cell-to-cell spread.
MeSH term(s)	Antibodies, Neutralizing/immunology ; Coculture Techniques ; Culture Media ; Cytokines/antagonists & inhibitors ; Cytokines/immunology ; Cytomegalovirus ; Epithelial Cells/drug effects ; Epithelial Cells/virology ; Humans ; Interferon Type I/immunology ; Interferon-beta/immunology ; Macrophages/immunology ; Macrophages/virology ; Tumor Necrosis Factor-alpha/immunology ; Virus Replication/drug effects
Chemical Substances	Antibodies, Neutralizing ; Culture Media ; Cytokines ; Interferon Type I ; Tumor Necrosis Factor-alpha ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2018-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2657572-3
ISSN	2150-5608 ; 2150-5594
ISSN (online)	2150-5608
ISSN	2150-5594
DOI	10.1080/21505594.2018.1535785
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Type I interferon receptor signaling delays Kupffer cell replenishment during acute fulminant viral hepatitis.

Borst, Katharina / Frenz, Theresa / Spanier, Julia / Tegtmeyer, Pia-Katharina / Chhatbar, Chintan / Skerra, Jennifer / Ghita, Luca / Namineni, Sukumar / Lienenklaus, Stefan / Köster, Mario / Heikenwaelder, Mathias / Sutter, Gerd / Kalinke, Ulrich

Journal of hepatology

2017 Volume 68, Issue 4, Page(s) 682–690

Abstract: Background & aim: Virus-induced fulminant hepatitis is a major cause of acute liver failure. During acute viral hepatitis the impact of type I interferon (IFN-I) on myeloid cells, including liver-resident Kupffer cells (KC), is only partially understood. ...

Abstract	Background & aim: Virus-induced fulminant hepatitis is a major cause of acute liver failure. During acute viral hepatitis the impact of type I interferon (IFN-I) on myeloid cells, including liver-resident Kupffer cells (KC), is only partially understood. Herein, we dissected the impact of locally induced IFN-I responses on myeloid cell function and hepatocytes during acute liver inflammation. Methods: Two different DNA-encoded viruses, vaccinia virus (VACV) and murine cytomegalovirus (MCMV), were studied. In vivo imaging was applied to visualize local IFN-β induction and IFN-I receptor (IFNAR) triggering in VACV-infected reporter mice. Furthermore, mice with a cell type-selective IFNAR ablation were analyzed to dissect the role of IFNAR signaling in myeloid cells and hepatocytes. Experiments with Cx3cr1 Results: VACV infection induced local IFN-β responses, which lead to IFNAR signaling primarily within the liver. IFNAR triggering was needed to control the infection and prevent fulminant hepatitis. The severity of liver inflammation was independent of IFNAR triggering of hepatocytes, whereas IFNAR triggering of myeloid cells protected from excessive inflammation. Upon VACV or MCMV infection KC disappeared, whereas infiltrating monocytes differentiated to KC afterwards. During IFNAR triggering such replenished monocyte-derived KC comprised more IFNAR-deficient than -competent cells in mixed bone marrow chimeric mice, whereas after the decline of IFNAR triggering both subsets showed an even distribution. Conclusion: Upon VACV infection IFNAR triggering of myeloid cells, but not of hepatocytes, critically modulates acute viral hepatitis. During infection with DNA-encoded viruses IFNAR triggering of liver-infiltrating blood monocytes delays the development of monocyte-derived KC, pointing towards new therapeutic strategies for acute viral hepatitis. Lay summary: Viral infection can cause fulminant hepatitis, which in turn is a major cause of acute liver failure. Herein, we aimed to study the role of type 1 interferon responses in acute viral hepatitis. We identified that during infection with DNA-encoded viruses, type 1 interferon receptor triggering of blood monocytes delays the development of monocyte-derived Kupffer cells. This points to new therapeutic strategies for acute viral hepatitis.
MeSH term(s)	Acute Disease ; Animals ; Hepatitis, Viral, Animal/etiology ; Hepatitis, Viral, Animal/physiopathology ; Kupffer Cells/physiology ; Mice ; Mice, Inbred C57BL ; Receptor, Interferon alpha-beta/physiology ; Signal Transduction/physiology ; Vaccinia/physiopathology
Chemical Substances	Receptor, Interferon alpha-beta (156986-95-7)
Language	English
Publishing date	2017-12-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2017.11.029
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Nature communications

2019

Abstract	Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.
Subject code	570
Language	English
Publishing date	2019-06-27
Publisher	Springer-Nature
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: STING induces early IFN-β in the liver and constrains myeloid cell-mediated dissemination of murine cytomegalovirus.

Nature communications

2019

Abstract	Cytomegalovirus is a DNA-encoded β-herpesvirus that induces STING-dependent type 1 interferon responses in macrophages and uses myeloid cells as a vehicle for dissemination. Here we report that STING knockout mice are as resistant to murine cytomegalovirus (MCMV) infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection. Although STING alone is dispensable for survival, early IFN-β induction in Kupffer cells is STING-dependent and controls early hepatic virus propagation. Infection experiments with an inducible reporter MCMV show that STING constrains MCMV replication in myeloid cells and limits viral dissemination via these cells. By contrast, restriction of viral dissemination from hepatocytes to other organs is independent of STING. Thus, during MCMV infection STING is involved in early IFN-β induction in Kupffer cells and the restriction of viral dissemination via myeloid cells, whereas it is dispensable for survival.
Subject code	570
Language	English
Publishing date	2019-06-27
Publisher	Springer-Nature
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hepatocyte-specific suppression of microRNA-221-3p mitigates liver fibrosis.

Journal of hepatology

2018 Volume 70, Issue 4, Page(s) 722–734

Abstract: Background & aims: Fibrosis, a cardinal feature of a dysfunctional liver, significantly contributes to the ever-increasing mortality due to end-stage chronic liver diseases. The crosstalk between hepatocytes and hepatic stellate cells (HSCs) plays a key ...

Abstract	Background & aims: Fibrosis, a cardinal feature of a dysfunctional liver, significantly contributes to the ever-increasing mortality due to end-stage chronic liver diseases. The crosstalk between hepatocytes and hepatic stellate cells (HSCs) plays a key role in the progression of fibrosis. Although ample efforts have been devoted to elucidate the functions of HSCs during liver fibrosis, the regulatory functions of hepatocytes remain elusive. Methods: Using an unbiased functional microRNA (miRNA) screening, we investigated the ability of hepatocytes to regulate fibrosis by fine-tuning gene expression via miRNA modulation. The in vivo functional analyses were performed by inhibiting miRNA in hepatocytes using adeno-associated virus in carbon-tetrachloride- and 3,5-di-diethoxycarbonyl-1,4-dihydrocollidine-induced liver fibrosis. Results: Blocking miRNA-221-3p function in hepatocytes during chronic liver injury facilitated recovery of the liver and faster resolution of the deposited extracellular matrix. Furthermore, we demonstrate that reduced secretion of C-C motif chemokine ligand 2, as a result of post-transcriptional regulation of GNAI2 (G protein alpha inhibiting activity polypeptide 2) by miRNA-221-3p, mitigates liver fibrosis. Conclusions: Collectively, miRNA modulation in hepatocytes, an easy-to-target cell type in the liver, may serve as a potential therapeutic approach for liver fibrosis. Lay summary: Liver fibrosis majorly contributes to mortality resulting from various liver diseases. We discovered a small RNA known as miRNA-221-3p, whose downregulation in hepatocytes results in reduced liver fibrosis. Thus, inhibition of miRNA-221-3p may serve as one of the therapeutic approaches for treatment of liver fibrosis.
MeSH term(s)	Animals ; Carbon Tetrachloride/pharmacology ; Dependovirus/genetics ; Down-Regulation/genetics ; Extracellular Matrix/metabolism ; Female ; Gene Expression Regulation ; HEK293 Cells ; Hepatic Stellate Cells/metabolism ; Hepatocytes/metabolism ; Humans ; Liver Cirrhosis, Experimental/chemically induced ; Liver Cirrhosis, Experimental/metabolism ; Liver Cirrhosis, Experimental/pathology ; Mice ; Mice, Inbred BALB C ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Transfection
Chemical Substances	MIRN221 microRNA, human ; MIRN221 microRNA, mouse ; MicroRNAs ; Carbon Tetrachloride (CL2T97X0V0)
Language	English
Publishing date	2018-12-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2018.12.016
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Article ; Online: Human monocyte-derived macrophages inhibit HCMV spread independent of classical antiviral cytokines.

Virulence

2018

Abstract	Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To better understand HCMV pathogenesis we studied mechanisms that restrict HCMV spread. We discovered that HCMV-infected cells can directly trigger plasmacytoid dendritic cells (pDC) to mount antiviral type I interferon (IFN-I) responses, even in the absence of cell-free virus. In contrast, monocyte-derived cells only expressed IFN-I when stimulated by cell-free HCMV, or upon encounter of HCMV-infected cells that already produced cell-free virus. Nevertheless, also in the absence of cell-free virus, i.e., upon co-culture of infected epithelial/endothelial cells and monocyte-derived macrophages (moMΦ) or dendritic cells (moDC), antiviral responses were induced that limited HCMV spread. The induction of this antiviral effect was dependent on cell-cell contact, whereas cell-free supernatants from co-culture experiments also inhibited virus spread, implying that soluble factors were critically needed. Interestingly, the antiviral effect was independent of IFN-γ, TNF-α, and IFN-I as indicated by cytokine inhibition experiments using neutralizing antibodies or the vaccinia virus-derived soluble IFN-I binding protein B18R, which traps human IFN-α and IFN-β. In conclusion, our results indicate that human macrophages and dendritic cells can limit HCMV spread by IFN-I dependent as well as independent mechanisms, whereas the latter ones might be particularly relevant for the restriction of HCMV transmission via cell-to-cell spread.
Keywords	Human cytomegalovirus ; epithelial cells ; macrophages ; plasmacytoid dendritic cells ; type I interferons
Subject code	610 ; 570
Publishing date	2018-01-01
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Human monocyte-derived macrophages inhibit HCMV spread independent of classical antiviral cytokines.

Virulence

2018

Abstract	Infection of healthy individuals with human cytomegalovirus (HCMV) is usually unnoticed and results in life-long latency, whereas HCMV reactivation as well as infection of newborns or immunocompromised patients can cause life-threatening disease. To better understand HCMV pathogenesis we studied mechanisms that restrict HCMV spread. We discovered that HCMV-infected cells can directly trigger plasmacytoid dendritic cells (pDC) to mount antiviral type I interferon (IFN-I) responses, even in the absence of cell-free virus. In contrast, monocyte-derived cells only expressed IFN-I when stimulated by cell-free HCMV, or upon encounter of HCMV-infected cells that already produced cell-free virus. Nevertheless, also in the absence of cell-free virus, i.e., upon co-culture of infected epithelial/endothelial cells and monocyte-derived macrophages (moMΦ) or dendritic cells (moDC), antiviral responses were induced that limited HCMV spread. The induction of this antiviral effect was dependent on cell-cell contact, whereas cell-free supernatants from co-culture experiments also inhibited virus spread, implying that soluble factors were critically needed. Interestingly, the antiviral effect was independent of IFN-γ, TNF-α, and IFN-I as indicated by cytokine inhibition experiments using neutralizing antibodies or the vaccinia virus-derived soluble IFN-I binding protein B18R, which traps human IFN-α and IFN-β. In conclusion, our results indicate that human macrophages and dendritic cells can limit HCMV spread by IFN-I dependent as well as independent mechanisms, whereas the latter ones might be particularly relevant for the restriction of HCMV transmission via cell-to-cell spread.
Keywords	Human cytomegalovirus ; epithelial cells ; macrophages ; plasmacytoid dendritic cells ; type I interferons
Subject code	610 ; 570
Publishing date	2018-01-01
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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