LIVIVO - Search results -

Search results

Result 1 - 10 of total 40

Search options

Article ; Online: Autophagy Special Collection: Cell machinery dealing with stress and beyond.

Cunha, Larissa D

2022 Volume 8, Issue 43, Page(s) eadf0585

Language	English
Publishing date	2022-10-26
Publishing country	United States
Document type	Editorial
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adf0585
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: License to LAP.

Cunha, Larissa D

Cell host & microbe

2021 Volume 29, Issue 8, Page(s) 1216–1217

Abstract: Engagement of LC3-associated phagocytosis (LAP) in response to the uptake of certain particles modulates innate immune responses. Now in Cell Host and Microbe, Akoumianaki et al. (2021) show how a regulatory role of IL-6 on LAP may be at the core of ... ...

Abstract	Engagement of LC3-associated phagocytosis (LAP) in response to the uptake of certain particles modulates innate immune responses. Now in Cell Host and Microbe, Akoumianaki et al. (2021) show how a regulatory role of IL-6 on LAP may be at the core of susceptibility to secondary infection during severe sepsis.
MeSH term(s)	Autophagy ; Humans ; Immunity, Innate ; Microtubule-Associated Proteins ; Phagocytosis ; Phagosomes
Chemical Substances	Microtubule-Associated Proteins
Language	English
Publishing date	2021-08-12
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2021.07.010
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6578: 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)

Order via subito

Details ▾

Article ; Online: In vitro Assessment of Efferocytic Capacity of Human Macrophages Using Flow Cytometry.

Salina, Ana C G / Fortes-Rocha, Marlon / Cunha, Larissa D

Bio-protocol

2023 Volume 13, Issue 24, Page(s) e4903

Abstract: Clearance of dying cells, named efferocytosis, is a pivotal function of professional phagocytes that impedes the accumulation of cell debris. Efferocytosis can be experimentally assessed by differentially tagging the target cells and professional ... ...

Abstract	Clearance of dying cells, named efferocytosis, is a pivotal function of professional phagocytes that impedes the accumulation of cell debris. Efferocytosis can be experimentally assessed by differentially tagging the target cells and professional phagocytes and analyzing by cell imaging or flow cytometry. Here, we describe an assay to evaluate the uptake of apoptotic cells (ACs) by human macrophages in vitro by labeling the different cells with commercially available dyes and analysis by flow cytometry. We detail the methods to prepare and label human macrophages and apoptotic lymphocytes and the in vitro approach to determine AC uptake. This protocol is based on previously published literature and allows for in vitro modeling of the efficiency of AC engulfment during continual efferocytosis process. Also, it can be modified to evaluate the clearance of different cell types by diverse professional phagocytes.
Language	English
Publishing date	2023-12-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4903
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Recognition of Legionella pneumophila nucleic acids by innate immune receptors.

Cunha, Larissa D / Zamboni, Dario S

Microbes and infection

2014 Volume 16, Issue 12, Page(s) 985–990

Abstract: Innate immune receptors evolved to sense conserved molecules that are present in microbes or are released during non-physiological conditions. Activation of these receptors is essential for early restriction of microbial infections and generation of ... ...

Abstract	Innate immune receptors evolved to sense conserved molecules that are present in microbes or are released during non-physiological conditions. Activation of these receptors is essential for early restriction of microbial infections and generation of adaptive immunity. Among the conserved molecules sensed by innate immune receptors are the nucleic acids, which are abundantly contained in all infectious organisms including virus, bacteria, fungi and parasites. In this review we focus in the innate immune proteins that function to sense nucleic acids from the intracellular bacterial pathogen Legionella pneumophila and the importance of these processes to the outcome of the infection.
MeSH term(s)	Animals ; DNA, Bacterial/immunology ; Host-Pathogen Interactions ; Humans ; Immunity, Innate/physiology ; Inflammasomes/metabolism ; Interferon Type I/biosynthesis ; Legionella pneumophila/genetics ; Legionella pneumophila/immunology ; Legionnaires' Disease/genetics ; Legionnaires' Disease/immunology ; Legionnaires' Disease/metabolism ; Nucleic Acids/immunology ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; Toll-Like Receptor 9/metabolism ; Toll-Like Receptors/metabolism
Chemical Substances	DNA, Bacterial ; Inflammasomes ; Interferon Type I ; Nucleic Acids ; Receptors, Immunologic ; Toll-Like Receptor 9 ; Toll-Like Receptors
Language	English
Publishing date	2014-12
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2014.08.008
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5014: 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)

Order via subito

Details ▾

Article: Subversion of inflammasome activation and pyroptosis by pathogenic bacteria.

Cunha, Larissa D / Zamboni, Dario S

Frontiers in cellular and infection microbiology

2013 Volume 3, Page(s) 76

Abstract: Activation of the inflammasome occurs in response to a notably high number of pathogenic microbes and is a broad innate immune response that effectively contributes to restriction of pathogen replication and generation of adaptive immunity. Activation of ...

Abstract	Activation of the inflammasome occurs in response to a notably high number of pathogenic microbes and is a broad innate immune response that effectively contributes to restriction of pathogen replication and generation of adaptive immunity. Activation of these platforms leads to caspase-1- and/or caspase-11-dependent secretion of proteins, including cytokines, and induction of a specific form of cell death called pyroptosis, which directly or indirectly contribute for restriction of pathogen replication. Not surprisingly, bona fide intracellular pathogens developed strategies for manipulation of cell death to guarantee intracellular replication. In this sense, the remarkable advances in the knowledge of the inflammasome field have been accompanied by several reports characterizing the inhibition of this platform by several pathogenic bacteria. Herein, we review some processes used by pathogenic bacteria, including Yersinia spp., Pseudomonas aeruginosa, Vibrio parahaemolyticus, Chlamydia trachomatis, Francisella tularensis, Shigella flexneri, Legionella pneumophila, and Coxiella burnetii to evade the activation of the inflammasome and the induction of pyroptosis.
MeSH term(s)	Cell Death ; Gram-Negative Bacteria/growth & development ; Gram-Negative Bacteria/immunology ; Host-Pathogen Interactions ; Immune Evasion ; Inflammasomes/metabolism
Chemical Substances	Inflammasomes
Language	English
Publishing date	2013-11-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2619676-1
ISSN	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2013.00076
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Retraction Note: Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells.

Martinez, Jennifer / Cunha, Larissa D / Park, Sunmin / Yang, Mao / Lu, Qun / Orchard, Robert / Li, Quan-Zhen / Yan, Mei / Janke, Laura / Guy, Cliff / Linkermann, Andreas / Virgin, Herbert W / Green, Douglas R

Nature

2022 Volume 609, Issue 7927, Page(s) 640

Language	English
Publishing date	2022-08-31
Publishing country	England
Document type	Retraction of Publication
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-05201-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 26: 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.MG 9: Show issues
Zs.MO 244: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: LC3-Associated Phagocytosis and Inflammation

Heckmann, Bradlee L / Boada-Romero, Emilio / Cunha, Larissa D / Magne, Joelle / Green, Douglas R

Journal of molecular biology. 2017 Nov. 24, v. 429, no. 23

2017

Abstract: LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC3 (microtubule-associated protein 1A/1B–light chain 3) is conjugated to phagosome membranes using a portion of the canonical autophagy machinery. The impact of LAP to ... ...

Abstract	LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC3 (microtubule-associated protein 1A/1B–light chain 3) is conjugated to phagosome membranes using a portion of the canonical autophagy machinery. The impact of LAP to immune regulation is best characterized in professional phagocytes, in particular macrophages, where LAP has instrumental roles in the clearance of extracellular particles including apoptotic cells and pathogens. Binding of dead cells via receptors present on the macrophage surface results in the translocation of the autophagy machinery to the phagosome and ultimately LC3 conjugation. These events promote a rapid form of phagocytosis that produces an “immunologically silent” clearance of the apoptotic cells. Consequences of LAP deficiency include a decreased capacity to clear dying cells and the establishment of a lupus-like autoimmune disease in mice. The ability of LAP to attenuate autoimmunity likely occurs through the dampening of pro-inflammatory signals upon engulfment of dying cells and prevention of autoantigen presentation to other immune cells. However, it remains unclear how LAP shapes both the activation and outcome of the immune response at the molecular level. Herein, we provide a detailed review of LAP and its known roles in the immune response and provide further speculation on the putative mechanisms by which LAP may regulate immune function, perhaps through the metabolic reprogramming and polarization of macrophages.
Keywords	apoptosis ; autoimmune diseases ; autoimmunity ; autophagy ; immune response ; inflammation ; macrophages ; mice ; pathogens ; phagosomes ; receptors
Language	English
Dates of publication	2017-1124
Size	p. 3561-3576.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2017.08.012
Database	NAL-Catalogue (AGRICOLA)

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Bonn / Germany

Z 4' 63/108: Show issues

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: LC3-Associated Phagocytosis and Inflammation.

Heckmann, Bradlee L / Boada-Romero, Emilio / Cunha, Larissa D / Magne, Joelle / Green, Douglas R

Journal of molecular biology

2017 Volume 429, Issue 23, Page(s) 3561–3576

Abstract: LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC3 (microtubule-associated protein 1A/1B-light chain 3) is conjugated to phagosome membranes using a portion of the canonical autophagy machinery. The impact of LAP to ... ...

Abstract	LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC3 (microtubule-associated protein 1A/1B-light chain 3) is conjugated to phagosome membranes using a portion of the canonical autophagy machinery. The impact of LAP to immune regulation is best characterized in professional phagocytes, in particular macrophages, where LAP has instrumental roles in the clearance of extracellular particles including apoptotic cells and pathogens. Binding of dead cells via receptors present on the macrophage surface results in the translocation of the autophagy machinery to the phagosome and ultimately LC3 conjugation. These events promote a rapid form of phagocytosis that produces an "immunologically silent" clearance of the apoptotic cells. Consequences of LAP deficiency include a decreased capacity to clear dying cells and the establishment of a lupus-like autoimmune disease in mice. The ability of LAP to attenuate autoimmunity likely occurs through the dampening of pro-inflammatory signals upon engulfment of dying cells and prevention of autoantigen presentation to other immune cells. However, it remains unclear how LAP shapes both the activation and outcome of the immune response at the molecular level. Herein, we provide a detailed review of LAP and its known roles in the immune response and provide further speculation on the putative mechanisms by which LAP may regulate immune function, perhaps through the metabolic reprogramming and polarization of macrophages.
MeSH term(s)	Animals ; Humans ; Inflammation/physiopathology ; Microtubule-Associated Proteins/metabolism ; Phagocytosis/physiology
Chemical Substances	MAP1LC3A protein, human ; Map1lc3b protein, mouse ; Microtubule-Associated Proteins
Language	English
Publishing date	2017-08-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2017.08.012
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 867: 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)

Order via subito

Details ▾

Article ; Online: Caspase-1 but Not Caspase-11 Is Required for NLRC4-Mediated Pyroptosis and Restriction of Infection by Flagellated Legionella Species in Mouse Macrophages and In Vivo.

Cerqueira, Daiane M / Pereira, Marcelo S F / Silva, Alexandre L N / Cunha, Larissa D / Zamboni, Dario S

Journal of immunology (Baltimore, Md. : 1950)

2015 Volume 195, Issue 5, Page(s) 2303–2311

Abstract: Gram-negative bacteria from the Legionella genus are intracellular pathogens that cause a severe form of pneumonia called Legionnaires' disease. The bacteria replicate intracellularly in macrophages, and the restriction of bacterial replication by these ... ...

Abstract	Gram-negative bacteria from the Legionella genus are intracellular pathogens that cause a severe form of pneumonia called Legionnaires' disease. The bacteria replicate intracellularly in macrophages, and the restriction of bacterial replication by these cells is critical for host resistance. The activation of the NAIP5/NLRC4 inflammasome, which is readily triggered in response to bacterial flagellin, is essential for the restriction of bacterial replication in murine macrophages. Once activated, this inflammasome induces pore formation and pyroptosis and facilitates the restriction of bacterial replication in macrophages. Because investigations related to the NLRC4-mediated restriction of Legionella replication were performed using mice double deficient for caspase-1 and caspase-11, we assessed the participation of caspase-1 and caspase-11 in the functions of the NLRC4 inflammasome and the restriction of Legionella replication in macrophages and in vivo. By using several species of Legionella and mice singly deficient for caspase-1 or caspase-11, we demonstrated that caspase-1 but not caspase-11 was required for pore formation, pyroptosis, and restriction of Legionella replication in macrophages and in vivo. By generating F1 mice in a mixed 129 × C57BL/6 background deficient (129 × Casp-11(-/-) ) or sufficient (129 × C57BL/6) for caspase-11 expression, we found that caspase-11 was dispensable for the restriction of Legionella pneumophila replication in macrophages and in vivo. Thus, although caspase-11 participates in flagellin-independent noncanonical activation of the NLRP3 inflammasome, it is dispensable for the activities of the NLRC4 inflammasome. In contrast, functional caspase-1 is necessary and sufficient to trigger flagellin/NLRC4-mediated restriction of Legionella spp. infection in macrophages and in vivo.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/immunology ; Apoptosis Regulatory Proteins/metabolism ; Blotting, Western ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/immunology ; Calcium-Binding Proteins/metabolism ; Caspase 1/genetics ; Caspase 1/immunology ; Caspase 1/metabolism ; Caspases/genetics ; Caspases/immunology ; Caspases/metabolism ; Cell Line ; Cells, Cultured ; Enzyme Activation/immunology ; Flagella/immunology ; Host-Pathogen Interactions/immunology ; Interleukin-1beta/biosynthesis ; Interleukin-1beta/immunology ; Legionella/classification ; Legionella/immunology ; Legionella/physiology ; Legionella pneumophila/immunology ; Legionella pneumophila/physiology ; Legionnaires' Disease/genetics ; Legionnaires' Disease/immunology ; Legionnaires' Disease/microbiology ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/microbiology ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Fluorescence ; Pyroptosis/genetics ; Pyroptosis/immunology ; Species Specificity
Chemical Substances	Apoptosis Regulatory Proteins ; Calcium-Binding Proteins ; Interleukin-1beta ; Ipaf protein, mouse ; Casp11 protein, mouse (EC 3.4.22.-) ; Caspases (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2015-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1501223
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: 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 28: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: CASP4/11 Contributes to NLRP3 Activation and COVID-19 Exacerbation.

Rodrigues, Tamara S / Caetano, Camila C S / de Sá, Keyla S G / Almeida, Leticia / Becerra, Amanda / Gonçalves, Augusto V / Lopes, Leticia de Sousa / Oliveira, Samuel / Mascarenhas, Danielle P A / Batah, Sabrina S / Silva, Bruna M / Gomes, Giovanni F / Castro, Ricardo / Martins, Ronaldo B / Avila, Jonathan / Frantz, Fabiani G / Cunha, Thiago M / Arruda, Eurico / Cunha, Fernando Q /

Nakaya, Helder / Cunha, Larissa D / Fabro, Alexandre T / Louzada-Junior, Paulo / de Oliveira, Renê D R / Zamboni, Dario S

The Journal of infectious diseases

2023 Volume 227, Issue 12, Page(s) 1364–1375

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection triggers activation of the NLRP3 inflammasome, which promotes inflammation and aggravates severe COVID-19. Here, we report that SARS-CoV-2 induces upregulation and activation of human ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection triggers activation of the NLRP3 inflammasome, which promotes inflammation and aggravates severe COVID-19. Here, we report that SARS-CoV-2 induces upregulation and activation of human caspase-4/CASP4 (mouse caspase-11/CASP11), and this process contributes to NLRP3 activation. In vivo infections performed in transgenic hACE2 humanized mice, deficient or sufficient for Casp11, indicate that hACE2 Casp11-/- mice were protected from disease development, with the increased pulmonary parenchymal area, reduced clinical score of the disease, and reduced mortality. Assessing human samples from fatal cases of COVID-19, we found that CASP4 was expressed in patient lungs and correlated with the expression of inflammasome components and inflammatory mediators, including CASP1, IL1B, IL18, and IL6. Collectively, our data establish that CASP4/11 promotes NLRP3 activation and disease pathology, revealing a possible target for therapeutic interventions for COVID-19.
MeSH term(s)	Mice ; Animals ; Humans ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Macrophages/metabolism ; COVID-19/metabolism ; SARS-CoV-2/metabolism ; Mice, Transgenic
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2023-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiad037
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uh II Zs.50: 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 445: Show issues

Order via subito

Details ▾

To top

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Bonn / Germany

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito