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Article ; Online: Editorial: Type III interferons: Emerging roles beyond antiviral barrier defense.

Boulant, Steeve / Forero, Adriana / Santer, Deanna M / Broggi, Achille

2022 Volume 13, Page(s) 1030812

MeSH term(s)	Antiviral Agents ; Hepacivirus ; Interferons
Chemical Substances	Antiviral Agents ; interferon type III ; Interferons (9008-11-1)
Language	English
Publishing date	2022-09-14
Publishing country	Switzerland
Document type	Editorial ; 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.2022.1030812
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Type III interferons: Balancing tissue tolerance and resistance to pathogen invasion.

Broggi, Achille / Granucci, Francesca / Zanoni, Ivan

The Journal of experimental medicine

2019 Volume 217, Issue 1

Abstract: Type III IFNs, or IFN-λ, are the newest members of the IFN family and were long believed to play roles that were redundant with those of type I IFNs. However, IFN-λ displays unique traits that delineate them as primary protectors of barrier integrity at ... ...

Abstract	Type III IFNs, or IFN-λ, are the newest members of the IFN family and were long believed to play roles that were redundant with those of type I IFNs. However, IFN-λ displays unique traits that delineate them as primary protectors of barrier integrity at mucosal sites. This unique role stems both from the restricted expression of IFN-λ receptor, confined to epithelial cells and to a limited pool of immune cells, and from unique immunomodulatory properties of IFN-λ. Here, we discuss recent findings that establish the unique capacity of IFN-λ to act at the barriers of the host to balance tissue tolerance and immune resistance against viral and bacterial challenges.
MeSH term(s)	Animals ; Bacteria/immunology ; Epithelial Cells/immunology ; Epithelial Cells/microbiology ; Epithelial Cells/virology ; Humans ; Immune Tolerance/immunology ; Interferons/immunology ; Viruses/immunology
Chemical Substances	interferon type III ; Interferons (9008-11-1)
Keywords	covid19
Language	English
Publishing date	2019-12-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20190295
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ua VI Zs.107: 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.MG 45: Show issues

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Article ; Online: Microbe- and danger-induced inflammation.

Broggi, Achille / Granucci, Francesca

Molecular immunology

2015 Volume 63, Issue 2, Page(s) 127–133

Abstract: The ability of the immune system to give rise to an effective response against pathogens while maintaining tolerance towards self-tissues has always been an object of keen interest for immunologist. Over the years, different theories have been proposed ... ...

Abstract	The ability of the immune system to give rise to an effective response against pathogens while maintaining tolerance towards self-tissues has always been an object of keen interest for immunologist. Over the years, different theories have been proposed to explain if and how the immune system is able to discriminate between self and non-self, including the Infectious Non-self theory from Charles Janeway and Polly Matzinger's Danger theory. Nowadays we know Janeway's theory is largely true, however the immune system does respond to injured, stressed and necrotic cells releasing danger signals (DAMPs) with a potent inflammatory response. To avoid unwanted prolonged autoimmune reactions, though, danger-induced inflammation should be tightly regulated. In the present review we discuss how prototypic DAMPs are able to induce inflammation and the peculiarity of danger-induced inflammation, as opposed to a complete immune response to fight pathogen invasions.
MeSH term(s)	Animals ; Bacteria/immunology ; HMGB1 Protein/metabolism ; Humans ; Inflammasomes/metabolism ; Inflammation/immunology ; Inflammation/microbiology ; Inflammation/pathology ; Receptors, Pattern Recognition/metabolism ; Toll-Like Receptors/metabolism
Chemical Substances	HMGB1 Protein ; Inflammasomes ; Receptors, Pattern Recognition ; Toll-Like Receptors
Language	English
Publishing date	2015-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2014.06.037
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 166: Show issues

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Article: Interferon (IFN)-λ Takes the Helm: Immunomodulatory Roles of Type III IFNs.

Zanoni, Ivan / Granucci, Francesca / Broggi, Achille

Frontiers in immunology

2017 Volume 8, Page(s) 1661

Abstract: Type III interferons (IFNs) (or IFN-λ) are the latest addition to the IFN family. Even though they share little protein homology with type I IFN, both exhibit remarkable functional similarities: each can be induced in response to viral infections, and ... ...

Abstract	Type III interferons (IFNs) (or IFN-λ) are the latest addition to the IFN family. Even though they share little protein homology with type I IFN, both exhibit remarkable functional similarities: each can be induced in response to viral infections, and both lead to Janus kinases (JAK) and signal transducer and activator of transcription (STAT) activation. The JAK/STAT pathway induces antiviral responses and IFN-stimulated gene transcription. However, despite the similarities in their effector functions with type I IFNs, IFN-λ also has a non-redundant role in protecting barrier organs: epithelial cells preferentially produce IFN-λ rather than type I IFNs; and interferon lambda receptor 1 (IFNLR1), the specific receptor for IFN-λ, is highly expressed on cells of epithelial lineage. Thus far, IFN-λ has been considered mainly as an epithelial cytokine, which restricts viral replication in epithelial cells and constitutes an added layer of protection at mucosal sites. However, it is now increasingly recognized that IFNLR1 is expressed broadly, and that immune cells such as neutrophils and dendritic cells also respond to IFN-λ. Moreover, in many
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.01661
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: IFN-λ suppresses intestinal inflammation by non-translational regulation of neutrophil function.

Broggi, Achille / Tan, Yunhao / Granucci, Francesca / Zanoni, Ivan

Nature immunology

2017 Volume 18, Issue 10, Page(s) 1084–1093

Abstract: Interferon-λ (IFN-λ) is a central regulator of mucosal immunity; however, its signaling specificity relative to that of type I interferons is poorly defined. IFN-λ can induce antiviral interferon-stimulated genes (ISGs) in epithelia, while the effect of ... ...

Abstract	Interferon-λ (IFN-λ) is a central regulator of mucosal immunity; however, its signaling specificity relative to that of type I interferons is poorly defined. IFN-λ can induce antiviral interferon-stimulated genes (ISGs) in epithelia, while the effect of IFN-λ in non-epithelial cells remains unclear. Here we report that neutrophils responded to IFN-λ. We found that in addition to inducing ISG transcription, IFN-λ (but not IFN-β) specifically activated a translation-independent signaling pathway that diminished the production of reactive oxygen species and degranulation in neutrophils. In mice, IFN-λ was elicited by enteric viruses and acted on neutrophils to decrease oxidative stress and intestinal damage. Thus, IFN-λ acted as a unique immunomodulatory agent by modifying transcriptional and non-translational neutrophil responses, which might permit a controlled development of the inflammatory process.
MeSH term(s)	Animals ; Cluster Analysis ; Disease Models, Animal ; Gastroenteritis/etiology ; Gastroenteritis/metabolism ; Gastroenteritis/pathology ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Humans ; Interferon-gamma/metabolism ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/microbiology ; Intestinal Mucosa/pathology ; Intestines/immunology ; Intestines/pathology ; Mice ; Mice, Knockout ; Microbiota ; Neutrophils/immunology ; Neutrophils/metabolism ; Oxidative Stress ; Receptors, Cytokine/genetics ; Receptors, Cytokine/metabolism
Chemical Substances	Receptors, Cytokine ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2017-08-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni.3821
Database	MEDical Literature Analysis and Retrieval System OnLINE

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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: Microbe- and danger-induced inflammation

Broggi, Achille / Francesca Granucci

Molecular Immunology. 2015 Feb., v. 63

2015

Abstract	The ability of the immune system to give rise to an effective response against pathogens while maintaining tolerance towards self-tissues has always been an object of keen interest for immunologist. Over the years, different theories have been proposed to explain if and how the immune system is able to discriminate between self and non-self, including the Infectious Non-self theory from Charles Janeway and Polly Matzinger's Danger theory. Nowadays we know Janeway's theory is largely true, however the immune system does respond to injured, stressed and necrotic cells releasing danger signals (DAMPs) with a potent inflammatory response. To avoid unwanted prolonged autoimmune reactions, though, danger-induced inflammation should be tightly regulated. In the present review we discuss how prototypic DAMPs are able to induce inflammation and the peculiarity of danger-induced inflammation, as opposed to a complete immune response to fight pathogen invasions.
Keywords	immune response ; immune system ; inflammation ; pathogens
Language	English
Dates of publication	2015-02
Size	p. 127-133.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2014.06.037
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 166: Show issues

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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: Preparation of Single-cell Suspensions for Cytofluorimetric Analysis from Different Mouse Skin Regions.

Broggi, Achille / Cigni, Clara / Zanoni, Ivan / Granucci, Francesca

Journal of visualized experiments : JoVE

2016 , Issue 110, Page(s) e52589

Abstract: The skin is a barrier organ that interacts with the external environment. Being continuously exposed to potential microbial invasion, the dermis and epidermis home a variety of immune cells in both homeostatic and inflammatory conditions. Tools to obtain ...

Abstract	The skin is a barrier organ that interacts with the external environment. Being continuously exposed to potential microbial invasion, the dermis and epidermis home a variety of immune cells in both homeostatic and inflammatory conditions. Tools to obtain skin cell release for cytofluorimetric analyses are, therefore, very useful in order to study the complex network of immune cells residing in the skin and their response to microbial stimuli. Here, we describe an efficient methodology for the digestion of mouse skin to rapidly and efficiently obtain single-cell suspensions. This protocol allows maintenance of maximum cell viability without compromising surface antigen expression. We also describe how to take and digest skin samples from different anatomical locations, such as the ear, trunk, tail, and footpad. The obtained suspensions are then stained and analyzed by flow cytometry to discriminate between different leukocyte populations.
MeSH term(s)	Animals ; Biomarkers/metabolism ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Separation ; Collagenases/pharmacology ; Dendritic Cells/cytology ; Dendritic Cells/metabolism ; Epidermis/cytology ; Flow Cytometry/methods ; Macrophages/cytology ; Macrophages/metabolism ; Matrix Metalloproteinase 8/pharmacology ; Mice ; Skin/cytology ; Skin/drug effects ; Skin/metabolism ; Skin Physiological Phenomena ; Suspensions ; Thermolysin/pharmacology
Chemical Substances	Biomarkers ; Suspensions ; Collagenases (EC 3.4.24.-) ; collagenase 1 (EC 3.4.24.-) ; Thermolysin (EC 3.4.24.27) ; Matrix Metalloproteinase 8 (EC 3.4.24.34)
Language	English
Publishing date	2016-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/52589
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Preparation of single-cell suspensions for cytofluorimetric analysis from different mouse skin regions

Broggi, Achille / Cigni, Clara / Zanoni, Ivan / Granucci, Francesca

Journal of visualized experiments. 2016 Apr. 20, , no. 110

2016

Abstract	The skin is a barrier organ that interacts with the external environment. Being continuously exposed to potential microbial invasion, the dermis and epidermis home a variety of immune cells in both homeostatic and inflammatory conditions. Tools to obtain skin cell release for cytofluorimetric analyses are, therefore, very useful in order to study the complex network of immune cells residing in the skin and their response to microbial stimuli. Here, we describe an efficient methodology for the digestion of mouse skin to rapidly and efficiently obtain single-cell suspensions. This protocol allows maintenance of maximum cell viability without compromising surface antigen expression. We also describe how to take and digest skin samples from different anatomical locations, such as the ear, trunk, tail, and footpad. The obtained suspensions are then stained and analyzed by flow cytometry to discriminate between different leukocyte populations.
Keywords	cell viability ; dermis ; ears ; flow cytometry ; leukocytes ; mice ; surface antigens ; tail
Language	English
Dates of publication	2016-0420
Size	p. e52589.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/52589
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Zinc-dependent histone deacetylases drive neutrophil extracellular trap formation and potentiate local and systemic inflammation.

Poli, Valentina / Pui-Yan Ma, Victor / Di Gioia, Marco / Broggi, Achille / Benamar, Mehdi / Chen, Qian / Mazitschek, Ralph / Haggarty, Stephen J / Chatila, Talal A / Karp, Jeffrey M / Zanoni, Ivan

iScience

2021 Volume 24, Issue 11, Page(s) 103256

Abstract: Neutrophil extracellular traps (NETs) have been implicated in the pathogenesis of acute respiratory distress syndrome (ARDS) driven by viruses or bacteria, as well as in numerous immune-mediated disorders. Histone citrullination by the enzyme ... ...

Abstract	Neutrophil extracellular traps (NETs) have been implicated in the pathogenesis of acute respiratory distress syndrome (ARDS) driven by viruses or bacteria, as well as in numerous immune-mediated disorders. Histone citrullination by the enzyme peptidylarginine deiminase 4 (PAD4) and the consequent decondensation of chromatin are hallmarks in the induction of NETs. Nevertheless, additional histone modifications that may govern NETosis are largely overlooked. Herein, we show that histone deacetylases (HDACs) play critical roles in driving NET formation in human and mouse neutrophils. HDACs belonging to the zinc-dependent lysine deacetylases family are necessary to deacetylate histone H3, thus allowing the activity of PAD4 and NETosis. Of note, HDAC inhibition in mice protects against microbial-induced pneumonia and septic shock, decreasing NETosis and inflammation. Collectively, our findings illustrate a new fundamental step that governs the release of NETs and points to HDAC inhibitors as therapeutic agents that may be used to protect against ARDS and sepsis.
Language	English
Publishing date	2021-10-11
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.103256
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Zinc-dependent histone deacetylases drive neutrophil extracellular trap formation and potentiate local and systemic inflammation

Valentina Poli / Victor Pui-Yan Ma / Marco Di Gioia / Achille Broggi / Mehdi Benamar / Qian Chen / Ralph Mazitschek / Stephen J. Haggarty / Talal A. Chatila / Jeffrey M. Karp / Ivan Zanoni

iScience, Vol 24, Iss 11, Pp 103256- (2021)

2021

Abstract: Summary: Neutrophil extracellular traps (NETs) have been implicated in the pathogenesis of acute respiratory distress syndrome (ARDS) driven by viruses or bacteria, as well as in numerous immune-mediated disorders. Histone citrullination by the enzyme ... ...

Abstract	Summary: Neutrophil extracellular traps (NETs) have been implicated in the pathogenesis of acute respiratory distress syndrome (ARDS) driven by viruses or bacteria, as well as in numerous immune-mediated disorders. Histone citrullination by the enzyme peptidylarginine deiminase 4 (PAD4) and the consequent decondensation of chromatin are hallmarks in the induction of NETs. Nevertheless, additional histone modifications that may govern NETosis are largely overlooked. Herein, we show that histone deacetylases (HDACs) play critical roles in driving NET formation in human and mouse neutrophils. HDACs belonging to the zinc-dependent lysine deacetylases family are necessary to deacetylate histone H3, thus allowing the activity of PAD4 and NETosis. Of note, HDAC inhibition in mice protects against microbial-induced pneumonia and septic shock, decreasing NETosis and inflammation. Collectively, our findings illustrate a new fundamental step that governs the release of NETs and points to HDAC inhibitors as therapeutic agents that may be used to protect against ARDS and sepsis.
Keywords	Molecular biology ; Immunology ; Cell biology ; Functional aspects of cell biology ; Science ; Q
Subject code	572
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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