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Article ; Online: Human and mouse NAIP/NLRC4 inflammasome responses to bacterial infection

Egan, Marisa S. / Zhang, Jenna / Sin, Sŏn-hwa

Current Opinion in Microbiology. 2023 June, v. 73 p.102298-

2023

Abstract: Intracellular immune complexes known as inflammasomes sense breaches of cytosolic sanctity. Inflammasomes promote downstream proinflammatory events, including interleukin-1 (IL-1) family cytokine release and pyroptotic cell death. The nucleotide-binding ... ...

Abstract	Intracellular immune complexes known as inflammasomes sense breaches of cytosolic sanctity. Inflammasomes promote downstream proinflammatory events, including interleukin-1 (IL-1) family cytokine release and pyroptotic cell death. The nucleotide-binding leucine-rich repeat family, apoptosis inhibitory protein/nucleotide-binding leucine-rich repeat family, caspase recruitment domain (CARD) domain-containing protein 4 (NAIP/NLRC4) inflammasome is involved in a range of pathogenic and protective inflammatory processes in mammalian hosts. In particular, the NAIP/NLRC4 inflammasome responds to flagellin and components of the virulence-associated type III secretion (T3SS) apparatus in the host cytosol, thereby allowing it to be a critical mediator of host defense during bacterial infection. Notable species- and cell type-specific differences exist in NAIP/NLRC4 inflammasome responses to bacterial pathogens. With a focus on Salmonella enterica serovar Typhimurium as a model pathogen, we review differences between murine and human NAIP/NLRC4 inflammasome responses. Differences in NAIP/NLRC4 inflammasome responses across species and cell types may have arisen in part due to evolutionary pressures.
Keywords	Salmonella Typhimurium ; bacterial infections ; caspases ; cytosol ; flagellin ; humans ; inflammasomes ; interleukin-1 ; mice ; microbiology ; pathogens ; pyroptosis ; secretion ; NAIP ; NLRC4 ; CARD ; T3SS ; T4SS ; IL-1 ; PRR ; PAMP ; IEC
Language	English
Dates of publication	2023-06
Publishing place	Elsevier Ltd
Document type	Article ; Online
ZDB-ID	1418474-6
ISSN	1879-0364 ; 1369-5274
ISSN (online)	1879-0364
ISSN	1369-5274
DOI	10.1016/j.mib.2023.102298
Database	NAL-Catalogue (AGRICOLA)

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Article: Yersinia

Zhang, Jenna / Brodsky, Igor E / Shin, Sunny

bioRxiv : the preprint server for biology

2023

Abstract: ... ...

Abstract	Yersinia
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.24.525473
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Article ; Online: Yersinia

Zhang, Jenna / Brodsky, Igor E / Shin, Sunny

mBio

2023 Volume 14, Issue 5, Page(s) e0131023

Abstract: Importance: ... ...

Abstract	Importance: Yersinia
MeSH term(s)	Humans ; Animals ; Mice ; Yersinia ; Inflammasomes ; Yersinia pestis ; Yersinia pseudotuberculosis ; Plague
Chemical Substances	Inflammasomes
Language	English
Publishing date	2023-08-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.01310-23
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Article ; Online: Human and mouse NAIP/NLRC4 inflammasome responses to bacterial infection.

Egan, Marisa S / Zhang, Jenna / Shin, Sunny

Current opinion in microbiology

2023 Volume 73, Page(s) 102298

Abstract	Intracellular immune complexes known as inflammasomes sense breaches of cytosolic sanctity. Inflammasomes promote downstream proinflammatory events, including interleukin-1 (IL-1) family cytokine release and pyroptotic cell death. The nucleotide-binding leucine-rich repeat family, apoptosis inhibitory protein/nucleotide-binding leucine-rich repeat family, caspase recruitment domain (CARD) domain-containing protein 4 (NAIP/NLRC4) inflammasome is involved in a range of pathogenic and protective inflammatory processes in mammalian hosts. In particular, the NAIP/NLRC4 inflammasome responds to flagellin and components of the virulence-associated type III secretion (T3SS) apparatus in the host cytosol, thereby allowing it to be a critical mediator of host defense during bacterial infection. Notable species- and cell type-specific differences exist in NAIP/NLRC4 inflammasome responses to bacterial pathogens. With a focus on Salmonella enterica serovar Typhimurium as a model pathogen, we review differences between murine and human NAIP/NLRC4 inflammasome responses. Differences in NAIP/NLRC4 inflammasome responses across species and cell types may have arisen in part due to evolutionary pressures.
MeSH term(s)	Humans ; Mice ; Animals ; Inflammasomes/metabolism ; Leucine/metabolism ; Macrophages ; Calcium-Binding Proteins/metabolism ; Bacterial Infections ; Nucleotides ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/metabolism ; Mammals ; Neuronal Apoptosis-Inhibitory Protein/genetics ; Neuronal Apoptosis-Inhibitory Protein/metabolism
Chemical Substances	Inflammasomes ; Leucine (GMW67QNF9C) ; Calcium-Binding Proteins ; Nucleotides ; CARD Signaling Adaptor Proteins ; NLRC4 protein, human ; NAIP protein, human ; Neuronal Apoptosis-Inhibitory Protein
Language	English
Publishing date	2023-04-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1418474-6
ISSN	1879-0364 ; 1369-5274
ISSN (online)	1879-0364
ISSN	1369-5274
DOI	10.1016/j.mib.2023.102298
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Article ; Online: Salmonella enterica Serovar Typhimurium Induces NAIP/NLRC4- and NLRP3/ASC-Independent, Caspase-4-Dependent Inflammasome Activation in Human Intestinal Epithelial Cells.

Naseer, Nawar / Zhang, Jenna / Bauer, Renate / Constant, David A / Nice, Timothy J / Brodsky, Igor E / Rauch, Isabella / Shin, Sunny

Infection and immunity

2022 Volume 90, Issue 7, Page(s) e0066321

Abstract: Salmonella enterica serovar Typhimurium is a Gram-negative pathogen that causes diseases ranging from gastroenteritis to systemic infection and sepsis. Salmonella uses type III secretion systems (T3SS) to inject effectors into host cells. While these ... ...

Abstract	Salmonella enterica serovar Typhimurium is a Gram-negative pathogen that causes diseases ranging from gastroenteritis to systemic infection and sepsis. Salmonella uses type III secretion systems (T3SS) to inject effectors into host cells. While these effectors are necessary for bacterial invasion and intracellular survival, intracellular delivery of T3SS products also enables detection of translocated Salmonella ligands by cytosolic immune sensors. Some of these sensors form multimeric complexes called inflammasomes, which activate caspases that lead to interleukin-1 (IL-1) family cytokine release and pyroptosis. In particular, the Salmonella T3SS needle, inner rod, and flagellin proteins activate the NAIP/NLRC4 inflammasome in murine intestinal epithelial cells (IECs), which leads to restriction of bacterial replication and extrusion of infected IECs into the intestinal lumen, thereby preventing systemic dissemination of Salmonella. While these processes are quite well studied in mice, the role of the NAIP/NLRC4 inflammasome in human IECs remains unknown. Unexpectedly, we found the NAIP/NLRC4 inflammasome is dispensable for early inflammasome responses to Salmonella in both human IEC lines and enteroids. Additionally, NLRP3 and the adaptor protein ASC are not required for inflammasome activation in Caco-2 cells. Instead, we observed a necessity for caspase-4 and gasdermin D pore-forming activity in mediating inflammasome responses to Salmonella in Caco-2 cells. These findings suggest that unlike murine IECs, human IECs do not rely on NAIP/NLRC4 or NLRP3/ASC inflammasomes and instead primarily use caspase-4 to mediate inflammasome responses to Salmonella pathogenicity island 1 (SPI-1)-expressing Salmonella.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins ; CARD Signaling Adaptor Proteins ; Caco-2 Cells ; Calcium-Binding Proteins ; Caspases, Initiator ; Epithelial Cells/metabolism ; Humans ; Inflammasomes/metabolism ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Neuronal Apoptosis-Inhibitory Protein ; Salmonella typhimurium ; Serogroup
Chemical Substances	Apoptosis Regulatory Proteins ; CARD Signaling Adaptor Proteins ; Calcium-Binding Proteins ; Inflammasomes ; Ipaf protein, mouse ; NAIP protein, human ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRC4 protein, human ; NLRP3 protein, human ; Naip1 protein, mouse ; Neuronal Apoptosis-Inhibitory Protein ; Nlrp3 protein, mouse ; PYCARD protein, human ; Pycard protein, mouse ; CASP4 protein, human (EC 3.4.22.-) ; Casp4 protein, mouse (EC 3.4.22.-) ; Caspases, Initiator (EC 3.4.22.-)
Language	English
Publishing date	2022-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/iai.00663-21
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Article ; Online: Nanoengineered Granular Hydrogel Bioinks with Preserved Interconnected Microporosity for Extrusion Bioprinting.

Ataie, Zaman / Kheirabadi, Sina / Zhang, Jenna Wanjing / Kedzierski, Alexander / Petrosky, Carter / Jiang, Rhea / Vollberg, Christian / Sheikhi, Amir

Small (Weinheim an der Bergstrasse, Germany)

2022 Volume 18, Issue 37, Page(s) e2202390

Abstract: 3D bioprinting of granular hydrogels comprising discrete hydrogel microparticles (microgels) may overcome the intrinsic structural limitations of bulk (nanoporous) hydrogel bioinks, enabling the fabrication of modular thick tissue constructs. The ... ...

Abstract	3D bioprinting of granular hydrogels comprising discrete hydrogel microparticles (microgels) may overcome the intrinsic structural limitations of bulk (nanoporous) hydrogel bioinks, enabling the fabrication of modular thick tissue constructs. The additive manufacturing of granular scaffolds has predominantly relied on highly jammed microgels to render the particulate suspensions shear yielding and extrudable. This inevitably compromises void spaces between microgels (microporosity), defeating rapid cell penetration, facile metabolite and oxygen transfer, and cell viability. Here, this persistent bottleneck is overcome by programming microgels with reversible interfacial nanoparticle self-assembly, enabling the fabrication of nanoengineered granular bioinks (NGB) with well-preserved microporosity, enhanced printability, and shape fidelity. The microporous architecture of bioprinted NGB constructs permits immediate post-printing 3D cell seeding, which may expand the library of bioinks via circumventing the necessity of bioorthogonality for cell-laden scaffold formation. This work opens new opportunities for the 3D bioprinting of tissue engineering microporous scaffolds beyond the traditional biofabrication window.
MeSH term(s)	Bioprinting ; Hydrogels/chemistry ; Microgels ; Printing, Three-Dimensional ; Tissue Engineering ; Tissue Scaffolds/chemistry
Chemical Substances	Hydrogels ; Microgels
Language	English
Publishing date	2022-08-03
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2168935-0
ISSN	1613-6829 ; 1613-6810
ISSN (online)	1613-6829
ISSN	1613-6810
DOI	10.1002/smll.202202390
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Article ; Online: A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.

Matsuda, Rina / Sorobetea, Daniel / Zhang, Jenna / Peterson, Stefan T / Grayczyk, James P / Yost, Winslow / Apenes, Nicolai / Kovalik, Maria E / Herrmann, Beatrice / O'Neill, Rosemary J / Bohrer, Andrea C / Lanza, Matthew / Assenmacher, Charles-Antoine / Mayer-Barber, Katrin D / Shin, Sunny / Brodsky, Igor E

The Journal of experimental medicine

2024 Volume 221, Issue 3

Abstract: Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the ... ...

Abstract	Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the intestinal mucosa and induces the recruitment of neutrophils and inflammatory monocytes into organized immune structures termed pyogranulomas (PG) that control Yersinia infection. Inflammatory monocytes are essential for the control and clearance of Yersinia within intestinal PG, but how monocytes mediate Yersinia restriction is poorly understood. Here, we demonstrate that TNF signaling in monocytes is required for bacterial containment following enteric Yersinia infection. We further show that monocyte-intrinsic TNFR1 signaling drives the production of monocyte-derived interleukin-1 (IL-1), which signals through IL-1 receptors on non-hematopoietic cells to enable PG-mediated control of intestinal Yersinia infection. Altogether, our work reveals a monocyte-intrinsic TNF-IL-1 collaborative inflammatory circuit that restricts intestinal Yersinia infection.
MeSH term(s)	Humans ; Interleukin-1 ; Yersinia ; Yersinia Infections ; Yersinia pseudotuberculosis ; Tumor Necrosis Factor-alpha ; Monocytes
Chemical Substances	Interleukin-1 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20230679
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Article: The tetrapeptide sequence of IL-1β regulates its recruitment and activation by inflammatory caspases.

Exconde, Patrick M / Hernandez-Chavez, Claudia / Bray, Mark B / Lopez, Jan L / Srivastava, Tamanna / Egan, Marisa S / Zhang, Jenna / Shin, Sunny / Discher, Bohdana M / Taabazuing, Cornelius Y

bioRxiv : the preprint server for biology

2023

Abstract: The mammalian innate immune system uses germline-encoded cytosolic pattern-recognition receptors (PRRs) to detect intracellular danger signals. At least six of these PRRs are known to form multiprotein complexes called inflammasomes which activate ... ...

Abstract	The mammalian innate immune system uses germline-encoded cytosolic pattern-recognition receptors (PRRs) to detect intracellular danger signals. At least six of these PRRs are known to form multiprotein complexes called inflammasomes which activate cysteine proteases known as caspases. Canonical inflammasomes recruit and activate caspase-1 (CASP1), which in turn cleaves and activates inflammatory cytokines such as IL-1β and IL-18, as well as the pore forming protein, gasdermin D (GSDMD), to induce pyroptotic cell death. In contrast, non-canonical inflammasomes, caspases-4/-5 (CASP4/5) in humans and caspase-11 (CASP11) in mice, are activated by intracellular LPS to cleave GSDMD, but their role in direct processing of inflammatory cytokines has not been established. Here we show that active CASP4/5 directly cleave IL-18 to generate the active species. Surprisingly, we also discovered that CASP4/5/11 cleave IL-1β at D27 to generate a 27 kDa fragment that is predicted to be inactive and cannot signal to the IL-1 receptor. Mechanistically, we discovered that the sequence identity of the P4-P1 tetrapeptide sequence adjacent to the caspase cleavage site (D116) regulates the recruitment and processing of IL-1β by inflammatory caspases to generate the bioactive species. Thus, we have identified new substrates of the non-canonical inflammasomes and reveal key mechanistic details regulating inflammation.
Language	English
Publishing date	2023-02-16
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.16.528859
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Article ; Online: The tetrapeptide sequence of IL-18 and IL-1β regulates their recruitment and activation by inflammatory caspases.

Exconde, Patrick M / Hernandez-Chavez, Claudia / Bourne, Christopher M / Richards, Rachel M / Bray, Mark B / Lopez, Jan L / Srivastava, Tamanna / Egan, Marisa S / Zhang, Jenna / Yoo, William / Shin, Sunny / Discher, Bohdana M / Taabazuing, Cornelius Y

Cell reports

2023 Volume 42, Issue 12, Page(s) 113581

Abstract: Inflammasomes are multiprotein signaling complexes that activate the innate immune system. Canonical inflammasomes recruit and activate caspase-1, which then cleaves and activates IL-1β and IL-18, as well as gasdermin D (GSDMD) to induce pyroptosis. In ... ...

Abstract	Inflammasomes are multiprotein signaling complexes that activate the innate immune system. Canonical inflammasomes recruit and activate caspase-1, which then cleaves and activates IL-1β and IL-18, as well as gasdermin D (GSDMD) to induce pyroptosis. In contrast, non-canonical inflammasomes, caspases-4/-5 (CASP4/5) in humans and caspase-11 (CASP11) in mice, are known to cleave GSDMD, but their role in direct processing of other substrates besides GSDMD has remained unknown. Here, we show that CASP4/5 but not CASP11 can directly cleave and activate IL-18. However, CASP4/5/11 can all cleave IL-1β to generate a 27-kDa fragment that deactivates IL-1β signaling. Mechanistically, we demonstrate that the sequence identity of the tetrapeptide sequence adjacent to the caspase cleavage site regulates IL-18 and IL-1β recruitment and activation. Altogether, we have identified new substrates of the non-canonical inflammasomes and reveal key mechanistic details regulating inflammation that may aid in developing new therapeutics for immune-related disorders.
MeSH term(s)	Caspases/genetics ; Caspases/immunology ; Interleukin-18/chemistry ; Interleukin-18/genetics ; Interleukin-18/immunology ; Interleukin-1beta/chemistry ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; RAW 264.7 Cells ; HEK293 Cells ; HeLa Cells ; THP-1 Cells ; Humans ; Inflammasomes/immunology ; Signal Transduction/genetics ; Proteolysis ; Protein Binding ; Protein Multimerization ; Salmonella Infections/enzymology ; Salmonella Infections/immunology
Chemical Substances	Caspases (EC 3.4.22.-) ; Interleukin-18 ; Interleukin-1beta ; Inflammasomes
Language	English
Publishing date	2023-12-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113581
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Article: A TNF-IL-1 circuit controls

Matsuda, Rina / Sorobetea, Daniel / Zhang, Jenna / Peterson, Stefan T / Grayczyk, James P / Herrmann, Beatrice / Yost, Winslow / O'Neill, Rosemary / Bohrer, Andrea C / Lanza, Matthew / Assenmacher, Charles-Antoine / Mayer-Barber, Katrin D / Shin, Sunny / Brodsky, Igor E

bioRxiv : the preprint server for biology

2023

Abstract: Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. ...

Abstract	Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens.
Language	English
Publishing date	2023-04-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.21.537749
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