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Article ; Online: Impaired innate antiviral defenses in COVID-19: Causes, consequences and therapeutic opportunities.

Galani, Ioanna-Evdokia / Andreakos, Evangelos

2021 Volume 55, Page(s) 101522

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a recently emerged pathogen that has caused coronavirus disease 2019 (COVID-19), the worst pandemic of our times leading to tremendous loss of human life and unprecedented measures of social ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a recently emerged pathogen that has caused coronavirus disease 2019 (COVID-19), the worst pandemic of our times leading to tremendous loss of human life and unprecedented measures of social distancing. COVID-19 symptom manifestations range from asymptomatic disease to severe and lethal outcomes. Lack of previous exposure and immunity to SARS-CoV-2, and high infectivity of the virus have contributed to its broad spread across the globe. In the absence of specific adaptive immunity, innate immune mechanisms are crucial for efficient antiviral defenses and control of the infection. Accumulating evidence now suggests that the remarkable heterogeneity in COVID-19 disease manifestations is due to variable degrees of impairment of innate immune mechanisms. In this review, we summarize recent findings describing both viral and host intrinsic factors that have been linked to defective innate immune responses and account for severe COVID-19. We also discuss emerging therapeutic opportunities for targeting innate immunity for the treatment of COVID-19.
MeSH term(s)	Adaptive Immunity ; Antiviral Agents/therapeutic use ; COVID-19 ; Humans ; Immunity, Innate ; SARS-CoV-2
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2021-11-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1018141-6
ISSN	1096-3618 ; 1044-5323
ISSN (online)	1096-3618
ISSN	1044-5323
DOI	10.1016/j.smim.2021.101522
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Article ; Online: Protocol for influenza A virus infection of mice and viral load determination

Ioanna-Evdokia Galani / Vasiliki Triantafyllia / Evridiki-Evangelia Eleminiadou / Evangelos Andreakos

STAR Protocols, Vol 3, Iss 1, Pp 101151- (2022)

2022

Abstract: ... viruses.For complete details on the use and execution of this protocol, please refer to Galani et al ...

Abstract	Summary: Influenza A viruses (IAVs) are common respiratory viruses. Mouse models of IAV infection are valuable to study the mechanisms of IAV infection and pathology. Here, we present a detailed protocol for IAV infection of mice via intranasal administration. We detail the processing of mouse lung tissue and then describe the determination of viral load by several approaches including RNA, protein, or plaque-forming unit assays. This protocol may be adapted to other influenza strains or respiratory viruses.For complete details on the use and execution of this protocol, please refer to Galani et al. (2017).
Keywords	Flow Cytometry/Mass Cytometry ; Immunology ; Microbiology ; Microscopy ; Model Organisms ; Molecular Biology ; Science (General) ; Q1-390
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Protocol for influenza A virus infection of mice and viral load determination.

Galani, Ioanna-Evdokia / Triantafyllia, Vasiliki / Eleminiadou, Evridiki-Evangelia / Andreakos, Evangelos

STAR protocols

2022 Volume 3, Issue 1, Page(s) 101151

Abstract: ... For complete details on the use and execution of this protocol, please refer to Galani et al. (2017). ...

Abstract	Influenza A viruses (IAVs) are common respiratory viruses. Mouse models of IAV infection are valuable to study the mechanisms of IAV infection and pathology. Here, we present a detailed protocol for IAV infection of mice via intranasal administration. We detail the processing of mouse lung tissue and then describe the determination of viral load by several approaches including RNA, protein, or plaque-forming unit assays. This protocol may be adapted to other influenza strains or respiratory viruses. For complete details on the use and execution of this protocol, please refer to Galani et al. (2017).
MeSH term(s)	Humans ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A virus ; Influenza, Human ; Orthomyxoviridae Infections/pathology ; Viral Load
Language	English
Publishing date	2022-02-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2022.101151
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Article ; Online: Notch signaling in adipose tissue macrophages prevents diet-induced inflammation and metabolic dysregulation.

Siouti, Eleni / Salagianni, Maria / Manioudaki, Maria / Pavlos, Eleftherios / Klinakis, Apostolos / Galani, Ioanna-Evdokia / Andreakos, Evangelos

European journal of immunology

2024 , Page(s) e2350669

Abstract: The importance of macrophages in adipose tissue (AT) homeostasis and inflammation is well established. However, the potential cues that regulate their function remain incompletely understood. To bridge this important gap, we sought to characterize novel ... ...

Abstract	The importance of macrophages in adipose tissue (AT) homeostasis and inflammation is well established. However, the potential cues that regulate their function remain incompletely understood. To bridge this important gap, we sought to characterize novel pathways involved using a mouse model of diet-induced obesity. By performing transcriptomics analysis of AT macrophages (ATMs), we found that late-stage ATMs from high-fat diet mice presented with perturbed Notch signaling accompanied by robust proinflammatory and metabolic changes. To explore the hypothesis that the deregulated Notch pathway contributes to the development of AT inflammation and diet-induced obesity, we employed a genetic approach to abrogate myeloid Notch1 and Notch2 receptors. Our results revealed that the combined loss of Notch1 and Notch2 worsened obesity-related metabolic dysregulation. Body and AT weight gain was higher, blood glucose levels increased and metabolic parameters were substantially worsened in deficient mice fed high-fat diet. Moreover, serum insulin and leptin were elevated as were triglycerides. Molecular analysis of ATMs showed that deletion of Notch receptors escalated inflammation through the induction of an M1-like pro-inflammatory phenotype. Our findings thus support a protective role of myeloid Notch signaling in adipose tissue inflammation and metabolic dysregulation.
Language	English
Publishing date	2024-02-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202350669
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Zs.A 489: 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)
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Article ; Online: Neutrophil-derived Activin-A moderates their pro-NETotic activity and attenuates collateral tissue damage caused by Influenza A virus infection.

Divolis, Georgios / Synolaki, Evgenia / Doulou, Athanasia / Gavriil, Ariana / Giannouli, Christina C / Apostolidou, Anastasia / Foster, Martyn L / Matzuk, Martin M / Skendros, Panagiotis / Galani, Ioanna-Evdokia / Sideras, Paschalis

Frontiers in immunology

2024 Volume 15, Page(s) 1302489

Abstract: Background: Pre-neutrophils, while developing in the bone marrow, transcribe the : Methods: To address this issue, we developed a neutrophil-specific Activin-A-deficient animal model (: Results: We found that neutrophil-specific Activin-A ... ...

Abstract	Background: Pre-neutrophils, while developing in the bone marrow, transcribe the Methods: To address this issue, we developed a neutrophil-specific Activin-A-deficient animal model ( Results: We found that neutrophil-specific Activin-A deficiency led to exacerbated pulmonary inflammation and widespread hemorrhagic histopathology in the lungs of IAV-infected animals that was associated with an exuberant production of neutrophil extracellular traps (NETs). Moreover, deletion of the Activin-A receptor ALK4/ACVR1B in neutrophils exacerbated IAV-induced pathology as well, suggesting that neutrophils themselves are potential targets of Activin-A-mediated signaling. The pro-NETotic tendency of Activin-A-deficient neutrophils was further verified in the context of thioglycollate-induced peritonitis, a model characterized by robust peritoneal neutrophilia. Of importance, transcriptome analysis of Activin-A-deficient neutrophils revealed alterations consistent with a predisposition for NET release. Conclusion: Collectively, our data demonstrate that Activin-A, secreted by neutrophils upon their activation in the periphery, acts as a feedback mechanism to moderate their pro-NETotic tendency and limit the collateral tissue damage caused by neutrophil excess activation during the inflammatory response.
MeSH term(s)	Animals ; Mice ; Humans ; Neutrophils ; Lung/pathology ; Influenza A virus ; Pneumonia/metabolism ; Influenza, Human/pathology ; Activins/metabolism
Chemical Substances	Activins (104625-48-1)
Language	English
Publishing date	2024-02-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1302489
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Article ; Online: CD103 integrin identifies a high IL-10-producing FoxP3

Tagkareli, Sofia / Salagianni, Maria / Galani, Ioanna-Evdokia / Manioudaki, Maria / Pavlos, Eleftherios / Thanopoulou, Kalliopi / Andreakos, Evangelos

Allergy

2021 Volume 77, Issue 4, Page(s) 1150–1164

Abstract: Background: Although FoxP3: Methods: We used an established mouse model of allergic airway disease based on ovalbumin sensitization and challenge to analyze FoxP3: Results: We found that during resolution of allergic airway inflammation in mice > ... ...

Abstract	Background: Although FoxP3 Methods: We used an established mouse model of allergic airway disease based on ovalbumin sensitization and challenge to analyze FoxP3 Results: We found that during resolution of allergic airway inflammation in mice >50% of FoxP3 Conclusions: Our study identifies a novel regulatory T-cell population, defined by CD103 expression, programmed to prevent exuberant type 2 inflammation and keep homeostasis in the respiratory tract under control. This has important therapeutic implications.
MeSH term(s)	Animals ; Antigens, CD/immunology ; Cytokines/metabolism ; Forkhead Transcription Factors/metabolism ; Humans ; Hypersensitivity ; Inflammation/metabolism ; Integrin alpha Chains/immunology ; Integrins/metabolism ; Interleukin-10/metabolism ; Lung ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory
Chemical Substances	Antigens, CD ; Cytokines ; FOXP3 protein, human ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Integrin alpha Chains ; Integrins ; alpha E integrins ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2021-10-28
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.15144
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Uh III Zs.150: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 125: Show issues

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Article ; Online: Severity of neonatal influenza infection is driven by type I interferon and oxidative stress.

Kumova, Ogan K / Galani, Ioanna-Evdokia / Rao, Abhishek / Johnson, Hannah / Triantafyllia, Vasiliki / Matt, Stephanie M / Pascasio, Judy / Gaskill, Peter J / Andreakos, Evangelos / Katsikis, Peter D / Carey, Alison J

Mucosal immunology

2022 Volume 15, Issue 6, Page(s) 1309–1320

Abstract: Neonates exhibit increased susceptibility to respiratory viral infections, attributed to inflammation at the developing pulmonary air-blood interface. IFN I are antiviral cytokines critical to control viral replication, but also promote inflammation. ... ...

Abstract	Neonates exhibit increased susceptibility to respiratory viral infections, attributed to inflammation at the developing pulmonary air-blood interface. IFN I are antiviral cytokines critical to control viral replication, but also promote inflammation. Previously, we established a neonatal murine influenza virus (IV) model, which demonstrates increased mortality. Here, we sought to determine the role of IFN I in this increased mortality. We found that three-day-old IFNAR-deficient mice are highly protected from IV-induced mortality. In addition, exposure to IFNβ 24 h post IV infection accelerated death in WT neonatal animals but did not impact adult mortality. In contrast, IFN IIIs are protective to neonatal mice. IFNβ induced an oxidative stress imbalance specifically in primary neonatal IV-infected pulmonary type II epithelial cells (TIIEC), not in adult TIIECs. Moreover, neonates did not have an infection-induced increase in antioxidants, including a key antioxidant, superoxide dismutase 3, as compared to adults. Importantly, antioxidant treatment rescued IV-infected neonatal mice, but had no impact on adult morbidity. We propose that IFN I exacerbate an oxidative stress imbalance in the neonate because of IFN I-induced pulmonary TIIEC ROS production coupled with developmentally regulated, defective antioxidant production in response to IV infection. This age-specific imbalance contributes to mortality after respiratory infections in this vulnerable population.
MeSH term(s)	Animals ; Mice ; Antioxidants/metabolism ; Inflammation ; Interferon Type I/metabolism ; Interferon-beta ; Mice, Inbred C57BL ; Orthomyxoviridae Infections/physiopathology ; Oxidative Stress ; Animals, Newborn
Chemical Substances	Antioxidants ; Interferon Type I ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2022-11-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-022-00576-x
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Zs.A 6796: Show issues

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Article ; Online: Untuned antiviral immunity in COVID-19 revealed by temporal type I/III interferon patterns and flu comparison.

Galani, Ioanna-Evdokia / Rovina, Nikoletta / Lampropoulou, Vicky / Triantafyllia, Vasiliki / Manioudaki, Maria / Pavlos, Eleftherios / Koukaki, Evangelia / Fragkou, Paraskevi C / Panou, Vasiliki / Rapti, Vasiliki / Koltsida, Ourania / Mentis, Andreas / Koulouris, Nikolaos / Tsiodras, Sotirios / Koutsoukou, Antonia / Andreakos, Evangelos

Nature immunology

2020 Volume 22, Issue 1, Page(s) 32–40

Abstract: A central paradigm of immunity is that interferon (IFN)-mediated antiviral responses precede pro-inflammatory ones, optimizing host protection and minimizing collateral ... ...

Abstract	A central paradigm of immunity is that interferon (IFN)-mediated antiviral responses precede pro-inflammatory ones, optimizing host protection and minimizing collateral damage
MeSH term(s)	Antiviral Agents/immunology ; Antiviral Agents/metabolism ; COVID-19/genetics ; COVID-19/immunology ; COVID-19/virology ; Cytokines/genetics ; Cytokines/immunology ; Disease Progression ; Gene Expression/genetics ; Gene Expression/immunology ; Gene Expression Profiling/methods ; Humans ; Immunity/genetics ; Immunity/immunology ; Inflammation/genetics ; Inflammation/immunology ; Influenza, Human/genetics ; Influenza, Human/immunology ; Interferon Type I/genetics ; Interferon Type I/immunology ; Interferons/genetics ; Interferons/immunology ; Length of Stay ; Prognosis ; SARS-CoV-2/immunology ; SARS-CoV-2/physiology ; Viral Load/genetics ; Viral Load/immunology
Chemical Substances	Antiviral Agents ; Cytokines ; Interferon Type I ; interferon type III ; Interferons (9008-11-1)
Language	English
Publishing date	2020-12-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-020-00840-x
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Interferon lambda1/IL-29 and inorganic polyphosphate are novel regulators of neutrophil-driven thromboinflammation.

Chrysanthopoulou, Akrivi / Kambas, Konstantinos / Stakos, Dimitrios / Mitroulis, Ioannis / Mitsios, Alexandros / Vidali, Veroniki / Angelidou, Iliana / Bochenek, Magdalena / Arelaki, Stella / Arampatzioglou, Athanasios / Galani, Ioanna-Evdokia / Skendros, Panagiotis / Couladouros, Elias A / Konstantinides, Stavros / Andreakos, Evangelos / Schäfer, Katrin / Ritis, Konstantinos

The Journal of pathology

2017 Volume 243, Issue 1, Page(s) 111–122

Abstract: Neutrophils and neutrophil-released meshwork structures termed neutrophil extracellular traps (NETs) are major mediators of thromboinflammation and emerging targets for therapy, yet the mechanisms and pathways that control the role of neutrophils in ... ...

Abstract	Neutrophils and neutrophil-released meshwork structures termed neutrophil extracellular traps (NETs) are major mediators of thromboinflammation and emerging targets for therapy, yet the mechanisms and pathways that control the role of neutrophils in thromboinflammation remain poorly understood. Here, we explored the role of IFN-λ1/IL-29, a major antiviral cytokine recently shown to suppress the neutrophil migratory capacity, in prothrombotic and proNETotic functions of neutrophils. In an ex vivo human experimental setting of acute ST-segment elevation myocardial infarction (STEMI), we show that IFN-λ1/IL-29 hinders NET release and diminishes the amount of cytoplasmic TF in neutrophils. Since platelet-neutrophil interaction plays a major role in NET-induced thromboinflammation, we further studied how IFN-λ1/IL-29 may interrupt this interaction. In this context, we identified inorganic polyphosphate (polyP) as a platelet-derived NET inducer in STEMI. In arterial STEMI thrombi, polyP was present in platelets and in close proximity to NET remnants. PolyP release from activated platelets was dependent on thrombin present in infarcted artery plasma, resulting in NET formation by promoting mTOR inhibition and autophagy induction. The effect of polyP on mTOR inhibition was counteracted by IFN-λ1/IL-29 treatment, leading to inhibition of NET formation. Consistently, we show in an in vivo model of FeCl
MeSH term(s)	Animals ; Autophagy ; Blood Coagulation ; Blood Platelets/metabolism ; Case-Control Studies ; Chlorides ; Disease Models, Animal ; Extracellular Traps/metabolism ; Ferric Compounds ; Humans ; Inflammation/blood ; Inflammation/chemically induced ; Inflammation/prevention & control ; Interferons ; Interleukins/administration & dosage ; Interleukins/blood ; Male ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Platelet Activation ; Polyphosphates/blood ; ST Elevation Myocardial Infarction/blood ; ST Elevation Myocardial Infarction/diagnostic imaging ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Thrombin/metabolism ; Thrombosis/blood ; Thrombosis/chemically induced ; Thrombosis/prevention & control
Chemical Substances	Chlorides ; Ferric Compounds ; interferon-lambda, human ; IL28A protein, mouse ; Interleukins ; Polyphosphates ; Interferons (9008-11-1) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Thrombin (EC 3.4.21.5) ; ferric chloride (U38V3ZVV3V)
Language	English
Publishing date	2017-08-07
Publishing country	England
Document type	Journal Article
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.4935
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Book ; Online ; Thesis: Enhancing anti-tumor immunity to MHC class I-deficient tumors

Galani, Ioanna Evdokia [Verfasser]

role of regulatory T cells and type I IFN

2008

Author's details	presented by Ioanna Evdokia Galani
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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