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  1. Book ; Thesis: Die Auswirkungen von viral/bakteriellen Infektionen auf die alveoläre Homöostase

    Deinhardt-Emmer, Stefanie / Löffler, Bettina / Pletz, Mathias / Ludwig, Stephan

    2023  

    Institution Friedrich-Schiller-Universität Jena
    Author's details von Dr. med. Stefanie Deinhardt-Emmer
    Keywords Lungenentzündung ; Atemwegsinfektion ; Lungenbläschen
    Subject Alveolus pulmonis ; Lungenalveole ; Respiratorische Infektionskrankheit ; Pneumonie
    Language German ; English
    Size 145 Blätter, Illustrationen, Diagramme, 30 cm
    Publishing place Jena
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Habilitationsschrift, Friedrich-Schiller-Universität Jena, 2023
    Note Zeitschriftenaufsätze in englischer Sprache ; Kumulative Habilitationsschrift, enthält Zeitschriftenaufsätze. - Erteilung der Lehrbefähigung: 14.02.2023
    HBZ-ID HT030016945
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Thesis: Phäno- und genotypische Charakterisierung von Herpes-simplex-Virus-Patientenisolation zur Ermittlung der Empfindlichkeit gegenüber Virostatika

    Deinhardt-Emmer, Stefanie

    2011  

    Author's details von Stefanie Deinhardt
    Language German
    Size 102 Bl., Ill., graph. Darst.
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Jena, Univ., Diss., 2011
    HBZ-ID HT017070752
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: SARS-CoV-2 virus-like particle variants alpha and delta mimic the native viruses in their differential inflammasome activating potential.

    Bandyszewska, Magdalena / Ambrożek-Latecka, Magdalena / Hoser, Grażyna / Grzanka, Małgorzata / Hornung, Franziska / Deinhardt-Emmer, Stefanie / Skirecki, Tomasz

    Antiviral research

    2024  Volume 224, Page(s) 105857

    Abstract: The emerging SARS-CoV-2 variants are evolving to evade human immunity and differ in their pathogenicity. While evasion of the variants from adaptive immunity is widely investigated, there is a paucity of knowledge about their interactions with innate ... ...

    Abstract The emerging SARS-CoV-2 variants are evolving to evade human immunity and differ in their pathogenicity. While evasion of the variants from adaptive immunity is widely investigated, there is a paucity of knowledge about their interactions with innate immunity. Inflammasome assembly is one of the most potent mechanisms of the early innate response to viruses, but when it is inappropriate, it can perpetuate tissue damage. In this study, we focused on the capacity of SARS-CoV-2 Alpha and Delta variants to activate the NLRP3 inflammasome. We compared the macrophage activation, particularly the inflammasome formation, using Alpha- and Delta-spike virus-like particles (VLPs). We found that VLPs of both variants activated the inflammasome even without a priming step. Delta-spike VLPs had a significantly stronger effect on triggering pyroptosis and inflammasome assembly in THP-1 macrophages than did Alfa-spike VLPs. Cells treated with Delta VLPs showed greater cleavage of caspase-1 and IL-1β release. Furthermore, Delta VLPs induced stronger cytokine secretion from macrophages and caused essential impairment of mitochondrial respiration in comparison to Alpha VLPs. Additionally, infection of primary human monocyte-derived macrophages with the SARS-CoV-2 variants confirmed the observations in VLPs. Collectively, we revealed that SARS-CoV-2 Delta had a greater impact on the inflammasome activation, cell death and mitochondrial respiration in macrophages than did the Alpha variant. Importantly, the differential response to the SARS-CoV-2 variants can influence the efficacy of therapies targeting the host's innate immunity.
    MeSH term(s) Humans ; Inflammasomes/genetics ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism ; COVID-19/metabolism ; Macrophages
    Chemical Substances Inflammasomes
    Language English
    Publishing date 2024-03-05
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 306628-9
    ISSN 1872-9096 ; 0166-3542
    ISSN (online) 1872-9096
    ISSN 0166-3542
    DOI 10.1016/j.antiviral.2024.105857
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: SARS-CoV-2 Testing of Emergency Department Patients Using cobas

    Egerer, Renate / Edel, Birgit / Hornung, Franziska / Deinhardt-Emmer, Stefanie / Baier, Michael / Lewejohann, Jan-Christoph / Pfister, Wolfgang / Löffler, Bettina / Rödel, Jürgen

    Diagnostics (Basel, Switzerland)

    2023  Volume 13, Issue 13

    Abstract: Rapid testing for Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) of patients presenting to emergency departments (EDs) facilitates the decision for isolation on admission to hospital wards. Differences in the sensitivity of molecular assays ...

    Abstract Rapid testing for Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) of patients presenting to emergency departments (EDs) facilitates the decision for isolation on admission to hospital wards. Differences in the sensitivity of molecular assays have implications for diagnostic workflows. This study evaluated the performance of the cobas
    Language English
    Publishing date 2023-07-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662336-5
    ISSN 2075-4418
    ISSN 2075-4418
    DOI 10.3390/diagnostics13132245
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Influenza A virus selectively elevates prostaglandin E

    Jordan, Paul M / Günther, Kerstin / Nischang, Vivien / Ning, Yuping / Deinhardt-Emmer, Stefanie / Ehrhardt, Christina / Werz, Oliver

    iScience

    2023  Volume 27, Issue 1, Page(s) 108775

    Abstract: Respiratory influenza A virus (IAV) infections are major health concerns worldwide, where bacterial superinfections substantially increase morbidity and mortality. The underlying mechanisms of how IAV impairs host defense remain elusive. Macrophages are ... ...

    Abstract Respiratory influenza A virus (IAV) infections are major health concerns worldwide, where bacterial superinfections substantially increase morbidity and mortality. The underlying mechanisms of how IAV impairs host defense remain elusive. Macrophages are pivotal for the innate immune response and crucially regulate the entire inflammatory process, occurring as inflammatory M1- or pro-resolving M2-like phenotypes. Lipid mediators (LM), produced from polyunsaturated fatty acids by macrophages, are potent immune regulators and impact all stages of inflammation. Using LM metabololipidomics, we show that human pro-resolving M2-macrophages respond to IAV infections with specific and robust production of prostaglandin (PG)E
    Language English
    Publishing date 2023-12-26
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.108775
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Influenza Virus-Induced Paracrine Cellular Senescence of the Lung Contributes to Enhanced Viral Load.

    Schulz, Luise / Hornung, Franziska / Häder, Antje / Radosa, Lukáš / Brakhage, Axel A / Löffler, Bettina / Deinhardt-Emmer, Stefanie

    Aging and disease

    2023  Volume 14, Issue 4, Page(s) 1331–1348

    Abstract: Aging is a major risk factor associated with increased morbidity and mortality rates observed during respiratory infections. In this study, we investigated the role of influenza virus infections in the establishment of premature cellular senescence and ... ...

    Abstract Aging is a major risk factor associated with increased morbidity and mortality rates observed during respiratory infections. In this study, we investigated the role of influenza virus infections in the establishment of premature cellular senescence and paracrine macrophage-activated inflammation. We observed in our murine model a premature aging by the appearance of senescent cells in the lungs after 21 d of influenza A virus infection. By using murine ex vivo lung models, the influence of TNF-α on the establishment of cellular senescence was detectable. Our findings were proven by using conditioned media of infected human monocyte-derived macrophages on primary lung fibroblasts. Here, a distinct expression of senescence-associated parameters could be confirmed. Furthermore, senescent cells in the lungs strongly influenced subsequent viral infections. Our data demonstrated a higher viral load in senescent primary lung fibroblasts, indicating an intracellular effect on viral replication. Transcriptomic data revealed an increased regulation of JAK/STAT signaling in senescent IAV-infected cells accompanied with increased TRAIL expression. Additionally, senescent cells indicating low pH values, accelerating viral replication. Our study provides new insights into pathomechanisms of virus-induced cellular senescence. Hence, IAV infection induces premature senescence and subsequent infections in senescent cells lead to an increased viral replication.
    Language English
    Publishing date 2023-08-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2625789-0
    ISSN 2152-5250
    ISSN 2152-5250
    DOI 10.14336/AD.2023.0310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Influenza A virus selectively elevates prostaglandin E2 formation in pro-resolving macrophages

    Paul M. Jordan / Kerstin Günther / Vivien Nischang / Yuping Ning / Stefanie Deinhardt-Emmer / Christina Ehrhardt / Oliver Werz

    iScience, Vol 27, Iss 1, Pp 108775- (2024)

    2024  

    Abstract: Summary: Respiratory influenza A virus (IAV) infections are major health concerns worldwide, where bacterial superinfections substantially increase morbidity and mortality. The underlying mechanisms of how IAV impairs host defense remain elusive. ... ...

    Abstract Summary: Respiratory influenza A virus (IAV) infections are major health concerns worldwide, where bacterial superinfections substantially increase morbidity and mortality. The underlying mechanisms of how IAV impairs host defense remain elusive. Macrophages are pivotal for the innate immune response and crucially regulate the entire inflammatory process, occurring as inflammatory M1- or pro-resolving M2-like phenotypes. Lipid mediators (LM), produced from polyunsaturated fatty acids by macrophages, are potent immune regulators and impact all stages of inflammation. Using LM metabololipidomics, we show that human pro-resolving M2-macrophages respond to IAV infections with specific and robust production of prostaglandin (PG)E2 along with upregulation of cyclooxygenase-2 (COX-2), which persists after co-infection with Staphylococcus aureus. In contrast, cytokine/interferon production in macrophages was essentially unaffected by IAV infection, and the functionality of M1-macrophages was not influenced. Conclusively, IAV infection of M2-macrophages selectively elevates PGE2 formation, suggesting inhibition of the COX-2/PGE2 axis as strategy to limit IAV exacerbation.
    Keywords Immunology ; Virology ; Science ; Q
    Language English
    Publishing date 2024-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article: SARS-CoV-2 and its ORF3a, E and M viroporins activate inflammasome in human macrophages and induce of IL-1α in pulmonary epithelial and endothelial cells.

    Ambrożek-Latecka, Magdalena / Kozlowski, Piotr / Hoser, Grażyna / Bandyszewska, Magdalena / Hanusek, Karolina / Nowis, Dominika / Gołąb, Jakub / Grzanka, Małgorzata / Piekiełko-Witkowska, Agnieszka / Schulz, Luise / Hornung, Franziska / Deinhardt-Emmer, Stefanie / Kozlowska, Ewa / Skirecki, Tomasz

    Cell death discovery

    2024  Volume 10, Issue 1, Page(s) 191

    Abstract: Inflammasome assembly is a potent mechanism responsible for the host protection against pathogens, including viruses. When compromised, it can allow viral replication, while when disrupted, it can perpetuate pathological responses by IL-1 signaling and ... ...

    Abstract Inflammasome assembly is a potent mechanism responsible for the host protection against pathogens, including viruses. When compromised, it can allow viral replication, while when disrupted, it can perpetuate pathological responses by IL-1 signaling and pyroptotic cell death. SARS-CoV-2 infection was shown to activate inflammasome in the lungs of COVID-19 patients, however, potential mechanisms responsible for this response are not fully elucidated. In this study, we investigated the effects of ORF3a, E and M SARS-CoV-2 viroporins in the inflammasome activation in major populations of alveolar sentinel cells: macrophages, epithelial and endothelial cells. We demonstrated that each viroporin is capable of activation of the inflammasome in macrophages to trigger pyroptosis-like cell death and IL-1α release from epithelial and endothelial cells. Small molecule NLRP3 inflammasome inhibitors reduced IL-1 release but weakly affected the pyroptosis. Importantly, we discovered that while SARS-CoV-2 could not infect the pulmonary microvascular endothelial cells it induced IL-1α and IL-33 release. Together, these findings highlight the essential role of macrophages as the major inflammasome-activating cell population in the lungs and point to endothelial cell expressed IL-1α as a potential novel component driving the pulmonary immunothromobosis in COVID-19.
    Language English
    Publishing date 2024-04-25
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-024-01966-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The Transmission of SARS-CoV-2 Infection on the Ocular Surface and Prevention Strategies.

    Kitazawa, Koji / Deinhardt-Emmer, Stefanie / Inomata, Takenori / Deshpande, Sharvari / Sotozono, Chie

    Cells

    2021  Volume 10, Issue 4

    Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global health problem. Although the respiratory system is the main impaired organ, conjunctivitis is one of its common findings. However, it is not yet understood if SARS-CoV-2 can ... ...

    Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global health problem. Although the respiratory system is the main impaired organ, conjunctivitis is one of its common findings. However, it is not yet understood if SARS-CoV-2 can infect the eye and if the ocular surface can be a potential route of SARS-CoV-2 transmissions. Our review focuses on the viral entry mechanisms to give a better understanding of the interaction between SARS-CoV-2 and the eye. We highlighted findings that give evidence for multiple potential receptors of SARS-CoV-2 on the ocular surface. Additionally, we focused on data concerning the detection of viral RNA and its spike protein in the various ocular tissues from patients. However, the expression level seemed to be relatively low compared to the respiratory tissues as a result of a unique environment surrounding the ocular surface and the innate immune response of SARS-CoV-2. Nevertheless, our review suggests the ocular surface as a potential route for SARS-CoV-2 transmission, and as a result of this study we strongly recommend the protection of the eyes for ophthalmologists and patients at risk.
    MeSH term(s) COVID-19/metabolism ; COVID-19/pathology ; COVID-19/prevention & control ; COVID-19/transmission ; Eye/metabolism ; Eye/pathology ; Eye/virology ; Host-Pathogen Interactions ; Humans ; SARS-CoV-2/physiology ; Virus Internalization
    Language English
    Publishing date 2021-04-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10040796
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The Inflammatory Profile of Obesity and the Role on Pulmonary Bacterial and Viral Infections.

    Hornung, Franziska / Rogal, Julia / Loskill, Peter / Löffler, Bettina / Deinhardt-Emmer, Stefanie

    International journal of molecular sciences

    2021  Volume 22, Issue 7

    Abstract: Obesity is a globally increasing health problem, entailing diverse comorbidities such as infectious diseases. An obese weight status has marked effects on lung function that can be attributed to mechanical dysfunctions. Moreover, the alterations of ... ...

    Abstract Obesity is a globally increasing health problem, entailing diverse comorbidities such as infectious diseases. An obese weight status has marked effects on lung function that can be attributed to mechanical dysfunctions. Moreover, the alterations of adipocyte-derived signal mediators strongly influence the regulation of inflammation, resulting in chronic low-grade inflammation. Our review summarizes the known effects regarding pulmonary bacterial and viral infections. For this, we discuss model systems that allow mechanistic investigation of the interplay between obesity and lung infections. Overall, obesity gives rise to a higher susceptibility to infectious pathogens, but the pathogenetic process is not clearly defined. Whereas, viral infections often show a more severe course in obese patients, the same patients seem to have a survival benefit during bacterial infections. In particular, we summarize the main mechanical impairments in the pulmonary tract caused by obesity. Moreover, we outline the main secretory changes within the expanded adipose tissue mass, resulting in chronic low-grade inflammation. Finally, we connect these altered host factors to the influence of obesity on the development of lung infection by summarizing observations from clinical and experimental data.
    MeSH term(s) Adipocytes/metabolism ; Adipokines/metabolism ; Adiponectin ; Adipose Tissue ; Animals ; Anti-Inflammatory Agents/pharmacology ; Bacterial Infections/complications ; Bacterial Infections/microbiology ; Bacterial Infections/virology ; Cells, Cultured ; Comorbidity ; Female ; Humans ; Inflammation ; Leptin/physiology ; Lung/microbiology ; Lung/physiopathology ; Lung/virology ; Macrophages/metabolism ; Male ; Mice ; Obesity/complications ; Obesity/microbiology ; Obesity/virology ; Risk Factors ; Virus Diseases/complications ; Virus Diseases/microbiology ; Virus Diseases/virology
    Chemical Substances Adipokines ; Adiponectin ; Anti-Inflammatory Agents ; Leptin
    Language English
    Publishing date 2021-03-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22073456
    Database MEDical Literature Analysis and Retrieval System OnLINE

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