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Article ; Online: The FAM13A Long Isoform Regulates Cilia Movement and Co-ordination in Airway Mucociliary Transport.

Howes, Ashleigh / Rogerson, Clare / Belyaev, Nikolai / Karagyozova, Tina / Rapiteanu, Radu / Fradique, Ricardo / Pellicciotta, Nicola / Mayhew, David / Hurd, Catherine / Crotta, Stefania / Singh, Tanya / Dingwell, Kevin / Myatt, Anniek / Arad, Navot / Hasan, Hikmatyar / Bijlsma, Hielke / Panjwani, Aliza / Vijayan, Vinaya / Young, George /

Bridges, Angela / Petit-Frere, Sebastien / Betts, Joanna / Larminie, Chris / Smith, James C / Hessel, Edith M / Michalovich, David / Walport, Louise / Cicuta, Pietro / Powell, Andrew J / Beinke, Soren / Wack, Andreas

American journal of respiratory cell and molecular biology

2024

Abstract: ... SNPs in ... ...

Abstract	SNPs in the
Language	English
Publishing date	2024-05-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2024-0063OC
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Article ; Online: Influenza-induced monocyte-derived alveolar macrophages confer prolonged antibacterial protection.

Aegerter, Helena / Kulikauskaite, Justina / Crotta, Stefania / Patel, Harshil / Kelly, Gavin / Hessel, Edith M / Mack, Matthias / Beinke, Soren / Wack, Andreas

Nature immunology

2020 Volume 21, Issue 2, Page(s) 145–157

Abstract: Despite the prevalence and clinical importance of influenza, its long-term effect on lung immunity is unclear. Here we describe that following viral clearance and clinical recovery, at 1 month after infection with influenza, mice are better protected ... ...

Abstract	Despite the prevalence and clinical importance of influenza, its long-term effect on lung immunity is unclear. Here we describe that following viral clearance and clinical recovery, at 1 month after infection with influenza, mice are better protected from Streptococcus pneumoniae infection due to a population of monocyte-derived alveolar macrophages (AMs) that produce increased interleukin-6. Influenza-induced monocyte-derived AMs have a surface phenotype similar to resident AMs but display a unique functional, transcriptional and epigenetic profile that is distinct from resident AMs. In contrast, influenza-experienced resident AMs remain largely similar to naive AMs. Thus, influenza changes the composition of the AM population to provide prolonged antibacterial protection. Monocyte-derived AMs persist over time but lose their protective profile. Our results help to understand how transient respiratory infections, a common occurrence in human life, can constantly alter lung immunity by contributing monocyte-derived, recruited cells to the AM population.
MeSH term(s)	Animals ; Immunity, Innate/immunology ; Macrophages, Alveolar/immunology ; Mice ; Orthomyxoviridae Infections/immunology ; Pneumococcal Infections/immunology
Language	English
Publishing date	2020-01-13
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/s41590-019-0568-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)
Zs.MG 42: Show issues

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Article ; Online: Rhinovirus-induced Human Lung Tissue Responses Mimic Chronic Obstructive Pulmonary Disease and Asthma Gene Signatures.

Wronski, Sabine / Beinke, Soren / Obernolte, Helena / Belyaev, Nikolai N / Saunders, Ken A / Lennon, Mark G / Schaudien, Dirk / Braubach, Peter / Jonigk, Danny / Warnecke, Gregor / Zardo, Patrick / Fieguth, Hans-Gerd / Wilkens, Ludwig / Braun, Armin / Hessel, Edith M / Sewald, Katherina

American journal of respiratory cell and molecular biology

2021 Volume 65, Issue 5, Page(s) 544–554

Abstract: Human rhinovirus (RV) is a major risk factor for chronic obstructive pulmonary disease (COPD) and asthma exacerbations. The exploration of RV pathogenesis has been hampered by a lack of disease-relevant model systems. We performed a detailed ... ...

Abstract	Human rhinovirus (RV) is a major risk factor for chronic obstructive pulmonary disease (COPD) and asthma exacerbations. The exploration of RV pathogenesis has been hampered by a lack of disease-relevant model systems. We performed a detailed characterization of host responses to RV infection in human lung tissue
MeSH term(s)	Aged ; Antiviral Agents/pharmacology ; Asthma/genetics ; Asthma/pathology ; Bronchi/pathology ; Bronchi/physiology ; Epithelial Cells/pathology ; Epithelial Cells/virology ; Female ; Gene Expression Profiling ; Genome, Human ; Host-Pathogen Interactions/genetics ; Humans ; Isoxazoles/pharmacology ; Lung/physiology ; Lung/virology ; Male ; Middle Aged ; Phenylalanine/analogs & derivatives ; Phenylalanine/pharmacology ; Picornaviridae Infections/drug therapy ; Picornaviridae Infections/genetics ; Picornaviridae Infections/pathology ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/pathology ; Pyrrolidinones/pharmacology ; Rhinovirus/pathogenicity ; Valine/analogs & derivatives ; Valine/pharmacology
Chemical Substances	Antiviral Agents ; Isoxazoles ; Pyrrolidinones ; Phenylalanine (47E5O17Y3R) ; Valine (HG18B9YRS7) ; rupintrivir (RGE5K1Q5QW)
Language	English
Publishing date	2021-07-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2020-0337OC
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Article ; Online: Corrected Super-Resolution Microscopy Enables Nanoscale Imaging of Autofluorescent Lung Macrophages.

Ambrose, Ashley R / Dechantsreiter, Susanne / Shah, Rajesh / Montero, M Angeles / Quinn, Anne Marie / Hessel, Edith M / Beinke, Soren / Tannahill, Gillian M / Davis, Daniel M

Biophysical journal

2020 Volume 119, Issue 12, Page(s) 2403–2417

Abstract: Observing the cell surface and underlying cytoskeleton at nanoscale resolution using super-resolution microscopy has enabled many insights into cell signaling and function. However, the nanoscale dynamics of tissue-specific immune cells have been ... ...

Abstract	Observing the cell surface and underlying cytoskeleton at nanoscale resolution using super-resolution microscopy has enabled many insights into cell signaling and function. However, the nanoscale dynamics of tissue-specific immune cells have been relatively little studied. Tissue macrophages, for example, are highly autofluorescent, severely limiting the utility of light microscopy. Here, we report a correction technique to remove autofluorescent noise from stochastic optical reconstruction microscopy (STORM) data sets. Simulations and analysis of experimental data identified a moving median filter as an accurate and robust correction technique, which is widely applicable across challenging biological samples. Here, we used this method to visualize lung macrophages activated through Fc receptors by antibody-coated glass slides. Accurate, nanoscale quantification of macrophage morphology revealed that activation induced the formation of cellular protrusions tipped with MHC class I protein. These data are consistent with a role for lung macrophage protrusions in antigen presentation. Moreover, the tetraspanin protein CD81, known to mark extracellular vesicles, appeared in ring-shaped structures (mean diameter 93 ± 50 nm) at the surface of activated lung macrophages. Thus, a moving median filter correction technique allowed us to quantitatively analyze extracellular secretions and membrane structure in tissue-derived immune cells.
MeSH term(s)	Cell Membrane ; Lung ; Macrophages ; Microscopy ; Microtubules
Language	English
Publishing date	2020-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1016/j.bpj.2020.10.041
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Zs.A 235: 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 2: Show issues

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Article ; Online: Highly efficient genome editing in primary human bronchial epithelial cells differentiated at air-liquid interface.

Rapiteanu, Radu / Karagyozova, Tina / Zimmermann, Natalie / Singh, Kuljit / Wayne, Gareth / Martufi, Matteo / Belyaev, Nikolai N / Hessel, Edith M / Michalovich, David / Macarron, Ricardo / Rowan, Wendy C / Cairns, William J / Roger, Jan / Betts, Joanna / Beinke, Soren / Maratou, Klio

The European respiratory journal

2020 Volume 55, Issue 5

MeSH term(s)	Bronchi/cytology ; Cell Culture Techniques/methods ; Cell Differentiation/genetics ; Epithelial Cells/metabolism ; Gene Editing/methods ; Humans ; Respiratory Mucosa/metabolism
Language	English
Publishing date	2020-05-21
Publishing country	England
Document type	Letter
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.00950-2019
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Zs.A 2322: 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)
Zs.MO 292: Show issues

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Article ; Online: Intranasal Bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection.

Groeger, David / Schiavi, Elisa / Grant, Ray / Kurnik-Łucka, Magdalena / Michalovich, David / Williamson, Rick / Beinke, Soren / Kiely, Barry / Akdis, Cezmi A / Hessel, Edith M / Shanahan, Fergus / O' Mahony, Liam

EBioMedicine

2020 Volume 60, Page(s) 102981

Abstract: Background: Prophylactic strategies are urgently needed for prevention of severe inflammatory responses to respiratory viral infections. Bacterial-host interactions may modify the immune response to viral infections.: Methods: We examined the ... ...

Abstract	Background: Prophylactic strategies are urgently needed for prevention of severe inflammatory responses to respiratory viral infections. Bacterial-host interactions may modify the immune response to viral infections. Methods: We examined the contribution of Intranasal administration of two different Bifidobacterium longum strains or its isolated cell wall in controlling viral induced inflammation using a murine model of influenza infection. We monitored mortality and morbidity over a 10-day period and viral load, differential broncho alveolar lavage (BAL) fluid inflammatory cell counts, Lung tissue histology, BAL and serum cytokines, markers of vascular damage and cell death were quantified. Findings: Intranasal administration of Bifidobacterium longum35624® or its isolated cell wall prior to virus inoculation significantly reduced viral load within the lungs and significantly improved survival. Reduced viral load was associated with reduced lung injury as suggested by cell death and vascular leakage markers, a shift from neutrophil to macrophage recruitment, reduced inflammatory cytokine levels (including IL-6), reduced type 1 and 2 interferon levels, but increased levels of interferon-λ and surfactant protein D. These protective effects were maintained when the bifidobacterial cell wall preparation was administered 24 h after viral inoculation. The protective effects were also observed for the Bifidobacterium longumPB-VIR™ strain. Interpretation: Exposure to these bifidobacterial strains protect against the inflammatory sequelae and damage associated with uncontrolled viral replication within the lung. Funding: This work has been funded, in part, by a research grant from GlaxoSmithKline, PrecisionBiotics Group Ltd., Swiss National Science Foundation grants (project numbers CRSII3_154488, 310030_144219, 310030_127356 and 310030_144219) and Christine Kühne - Center for Allergy Research and Education (CK-CARE).
MeSH term(s)	Administration, Intranasal ; Animals ; Bifidobacterium longum/immunology ; Coinfection/immunology ; Coinfection/microbiology ; Coinfection/virology ; Cross Protection/immunology ; Cytokines/metabolism ; Disease Models, Animal ; Female ; Host-Pathogen Interactions/immunology ; Inflammation Mediators/metabolism ; Influenza A virus/immunology ; Mice ; Mortality ; Nasal Cavity/immunology ; Nasal Cavity/microbiology ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/metabolism ; Orthomyxoviridae Infections/mortality ; Orthomyxoviridae Infections/pathology ; Pneumonia, Viral/immunology ; Pneumonia, Viral/metabolism ; Pneumonia, Viral/mortality ; Pneumonia, Viral/pathology ; Prognosis
Chemical Substances	Cytokines ; Inflammation Mediators
Keywords	covid19
Language	English
Publishing date	2020-09-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2020.102981
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Zs.A 7090: Show issues

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Article ; Online: Intranasal Bifidobacterium longum protects against viral-induced lung inflammation and injury in a murine model of lethal influenza infection

David Groeger / Elisa Schiavi / Ray Grant / Magdalena Kurnik-Łucka / David Michalovich / Rick Williamson / Soren Beinke / Barry Kiely / Cezmi A Akdis / Edith M Hessel / Fergus Shanahan / Liam O’ Mahony

EBioMedicine, Vol 60, Iss , Pp 102981- (2020)

2020

Abstract	Background: Prophylactic strategies are urgently needed for prevention of severe inflammatory responses to respiratory viral infections. Bacterial-host interactions may modify the immune response to viral infections. Methods: We examined the contribution of Intranasal administration of two different Bifidobacterium longum strains or its isolated cell wall in controlling viral induced inflammation using a murine model of influenza infection. We monitored mortality and morbidity over a 10-day period and viral load, differential broncho alveolar lavage (BAL) fluid inflammatory cell counts, Lung tissue histology, BAL and serum cytokines, markers of vascular damage and cell death were quantified. Findings: Intranasal administration of Bifidobacterium longum 35624® or its isolated cell wall prior to virus inoculation significantly reduced viral load within the lungs and significantly improved survival. Reduced viral load was associated with reduced lung injury as suggested by cell death and vascular leakage markers, a shift from neutrophil to macrophage recruitment, reduced inflammatory cytokine levels (including IL-6), reduced type 1 and 2 interferon levels, but increased levels of interferon-λ and surfactant protein D. These protective effects were maintained when the bifidobacterial cell wall preparation was administered 24 h after viral inoculation. The protective effects were also observed for the Bifidobacterium longum PB-VIR™ strain. Interpretation: Exposure to these bifidobacterial strains protect against the inflammatory sequelae and damage associated with uncontrolled viral replication within the lung. Funding: This work has been funded, in part, by a research grant from GlaxoSmithKline, PrecisionBiotics Group Ltd., Swiss National Science Foundation grants (project numbers CRSII3_154488, 310030_144219, 310030_127356 and 310030_144219) and Christine Kühne – Center for Allergy Research and Education (CK-CARE).
Keywords	Influenza ; Probiotic ; Interferon ; Prevention ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: IFNλ is a potent anti-influenza therapeutic without the inflammatory side effects of IFNα treatment.

Davidson, Sophia / McCabe, Teresa M / Crotta, Stefania / Gad, Hans Henrik / Hessel, Edith M / Beinke, Soren / Hartmann, Rune / Wack, Andreas

EMBO molecular medicine

2016 Volume 8, Issue 9, Page(s) 1099–1112

Abstract: Influenza A virus (IAV)-induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFNαβ) and type III interferon (IFNλ) are potent antiviral cytokines with ... ...

Abstract	Influenza A virus (IAV)-induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFNαβ) and type III interferon (IFNλ) are potent antiviral cytokines with immunomodulatory potential, we assessed their efficacy as IAV treatments. IFNλ treatment of IAV-infected Mx1-positive mice lowered viral load and protected from disease. IFNα treatment also restricted IAV replication but exacerbated disease. IFNα treatment increased pulmonary proinflammatory cytokine secretion, innate cell recruitment and epithelial cell death, unlike IFNλ-treatment. IFNλ lacked the direct stimulatory activity of IFNα on immune cells. In epithelia, both IFNs induced antiviral genes but no inflammatory cytokines. Similarly, human airway epithelia responded to both IFNα and IFNλ by induction of antiviral genes but not of cytokines, while hPBMCs responded only to IFNα. The restriction of both IFNλ responsiveness and productive IAV replication to pulmonary epithelia allows IFNλ to limit IAV spread through antiviral gene induction in relevant cells without overstimulating the immune system and driving immunopathology. We propose IFNλ as a non-inflammatory and hence superior treatment option for human IAV infection.
MeSH term(s)	Animals ; Cell Death ; Cytokines/analysis ; Disease Models, Animal ; Epithelial Cells/physiology ; Humans ; Influenza A virus/isolation & purification ; Interferon-alpha/therapeutic use ; Interleukins/therapeutic use ; Leukocytes/immunology ; Lung/pathology ; Mice ; Orthomyxoviridae Infections/drug therapy ; Orthomyxoviridae Infections/pathology ; Orthomyxoviridae Infections/prevention & control ; Orthomyxoviridae Infections/virology ; Treatment Outcome ; Viral Load
Chemical Substances	Cytokines ; IFNL4 protein, human ; Interferon-alpha ; Interleukins
Keywords	covid19
Language	English
Publishing date	2016-09-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.201606413
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Zs.A 6784: Show issues

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Article: NF-KappaB1 p105 regulates Tpl-2 kinase

Beinke, Sören

Futura

2003 Volume 18, Issue 3, Page(s) 183

Language	German
Document type	Article
ZDB-ID	382906-6
ISSN	0179-6372
Database	Current Contents Medicine

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Zs.B 2980: Show issues

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Article ; Online: IFNλ is a potent anti‐influenza therapeutic without the inflammatory side effects of IFNα treatment

Sophia Davidson / Teresa M McCabe / Stefania Crotta / Hans Henrik Gad / Edith M Hessel / Soren Beinke / Rune Hartmann / Andreas Wack

EMBO Molecular Medicine, Vol 8, Iss 9, Pp 1099-

2016 Volume 1112

Abstract: Abstract Influenza A virus (IAV)‐induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFNαβ) and type III interferon (IFNλ) are potent antiviral cytokines with ... ...

Abstract	Abstract Influenza A virus (IAV)‐induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFNαβ) and type III interferon (IFNλ) are potent antiviral cytokines with immunomodulatory potential, we assessed their efficacy as IAV treatments. IFNλ treatment of IAV‐infected Mx1‐positive mice lowered viral load and protected from disease. IFNα treatment also restricted IAV replication but exacerbated disease. IFNα treatment increased pulmonary proinflammatory cytokine secretion, innate cell recruitment and epithelial cell death, unlike IFNλ‐treatment. IFNλ lacked the direct stimulatory activity of IFNα on immune cells. In epithelia, both IFNs induced antiviral genes but no inflammatory cytokines. Similarly, human airway epithelia responded to both IFNα and IFNλ by induction of antiviral genes but not of cytokines, while hPBMCs responded only to IFNα. The restriction of both IFNλ responsiveness and productive IAV replication to pulmonary epithelia allows IFNλ to limit IAV spread through antiviral gene induction in relevant cells without overstimulating the immune system and driving immunopathology. We propose IFNλ as a non‐inflammatory and hence superior treatment option for human IAV infection.
Keywords	immunopathology ; infection ; influenza ; interferon alpha ; interferon lambda ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
Subject code	610 ; 570
Language	English
Publishing date	2016-09-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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