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Article: An innate granuloma eradicates an environmental pathogen using

Harvest, Carissa K / Abele, Taylor J / Yu, Chen / Beatty, Cole J / Amason, Megan E / Billman, Zachary P / DePrizio, Morgan A / Lacey, Carolyn A / Maltez, Vivien I / Larson, Heather N / McGlaughon, Benjamin D / Saban, Daniel R / Montgomery, Stephanie A / Miao, Edward A

bioRxiv : the preprint server for biology

2023

Abstract: Granulomas often form around pathogens that cause chronic infections. Here, we discover a novel granuloma model in mice. ...

Abstract	Granulomas often form around pathogens that cause chronic infections. Here, we discover a novel granuloma model in mice.
Language	English
Publishing date	2023-03-09
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.07.531568
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Reassessing the Evolutionary Importance of Inflammasomes.

Maltez, Vivien I / Miao, Edward A

Journal of immunology (Baltimore, Md. : 1950)

2016 Volume 196, Issue 3, Page(s) 956–962

Abstract: Inflammasomes monitor the cytosol for microbial contamination or perturbation and, thus, are predicted to provide potent defense against infection. However, the compendium of data from murine infection models suggests that inflammasomes merely delay the ... ...

Abstract	Inflammasomes monitor the cytosol for microbial contamination or perturbation and, thus, are predicted to provide potent defense against infection. However, the compendium of data from murine infection models suggests that inflammasomes merely delay the course of disease, allowing the host time to mount an adaptive response. Interpretations of such results are confounded by inflammasome-evasion strategies of vertebrate-adapted pathogens. Conversely, environmental opportunistic pathogens have not evolved in the context of inflammasomes and, therefore, are less likely to evade them. Indeed, opportunistic pathogens do not normally cause disease in wild-type animals. Accordantly, the extreme virulence of two opportunistic bacterial pathogens, Burkholderia thailandensis and Chromobacterium violaceum, is fully counteracted by inflammasomes in murine models. This leads us to propose a new hypothesis: perhaps animals maintain inflammasomes over evolutionary time not to defend against vertebrate-adapted pathogens but instead to counteract infection by a plethora of undiscovered opportunistic pathogens residing in the environment.
MeSH term(s)	Animals ; Biological Evolution ; Humans ; Inflammasomes/immunology ; Mice
Chemical Substances	Inflammasomes
Language	English
Publishing date	2016-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
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.1502060
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Article ; Online: The β

Globig, Anna-Maria / Zhao, Steven / Roginsky, Jessica / Maltez, Vivien I / Guiza, Juan / Avina-Ochoa, Natalia / Heeg, Maximilian / Araujo Hoffmann, Filipe / Chaudhary, Omkar / Wang, Jiawei / Senturk, Gokhan / Chen, Dan / O'Connor, Carolyn / Pfaff, Samuel / Germain, Ronald N / Schalper, Kurt A / Emu, Brinda / Kaech, Susan M

Nature

2023 Volume 622, Issue 7982, Page(s) 383–392

Abstract: ... ...

Abstract	CD8
MeSH term(s)	Humans ; Antigens/immunology ; Antigens/metabolism ; Catecholamines/metabolism ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Proliferation ; Immune Checkpoint Inhibitors/therapeutic use ; Melanoma/immunology ; Melanoma/metabolism ; Melanoma/therapy ; Memory T Cells/cytology ; Memory T Cells/immunology ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/therapy ; Receptors, Adrenergic, beta-1/metabolism ; Sympathetic Nervous System/immunology ; Sympathetic Nervous System/physiology ; T-Cell Exhaustion ; Stress, Physiological
Chemical Substances	ADRB1 protein, human ; Antigens ; Catecholamines ; Immune Checkpoint Inhibitors ; Receptors, Adrenergic, beta-1
Language	English
Publishing date	2023-09-20
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06568-6
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Article ; Online: NAIP inflammasomes give the NOD to bacterial ligands.

Maltez, Vivien I / Miao, Edward A

Trends in immunology

2014 Volume 35, Issue 11, Page(s) 503–504

Abstract: NLRs are innate immune sensors that monitor the sanctity of the cytosolic compartment. In a recent paper in Molecular Cell, Tenthorey et al. reveal a novel ligand-sensing interface within regions of the oligomerization domain of the NAIPs, rather than ... ...

Abstract	NLRs are innate immune sensors that monitor the sanctity of the cytosolic compartment. In a recent paper in Molecular Cell, Tenthorey et al. reveal a novel ligand-sensing interface within regions of the oligomerization domain of the NAIPs, rather than within the leucine-rich repeats, as was anticipated.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/metabolism ; Bacterial Proteins/metabolism ; Calcium-Binding Proteins/metabolism ; Humans ; Inflammasomes/metabolism ; Neuronal Apoptosis-Inhibitory Protein/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; Bacterial Proteins ; Calcium-Binding Proteins ; Inflammasomes ; Neuronal Apoptosis-Inhibitory Protein
Language	English
Publishing date	2014-11
Publishing country	England
Document type	Comment ; Journal Article
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2014.10.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: An innate granuloma eradicates an environmental pathogen using Gsdmd and Nos2.

Harvest, Carissa K / Abele, Taylor J / Yu, Chen / Beatty, Cole J / Amason, Megan E / Billman, Zachary P / DePrizio, Morgan A / Souza, Fernando W / Lacey, Carolyn A / Maltez, Vivien I / Larson, Heather N / McGlaughon, Benjamin D / Saban, Daniel R / Montgomery, Stephanie A / Miao, Edward A

Nature communications

2023 Volume 14, Issue 1, Page(s) 6686

Abstract: Granulomas often form around pathogens that cause chronic infections. Here, we discover an innate granuloma model in mice with an environmental bacterium called Chromobacterium violaceum. Granuloma formation not only successfully walls off, but also ... ...

Abstract	Granulomas often form around pathogens that cause chronic infections. Here, we discover an innate granuloma model in mice with an environmental bacterium called Chromobacterium violaceum. Granuloma formation not only successfully walls off, but also clears, the infection. The infected lesion can arise from a single bacterium that replicates despite the presence of a neutrophil swarm. Bacterial replication ceases when macrophages organize around the infection and form a granuloma. This granuloma response is accomplished independently of adaptive immunity that is typically required to organize granulomas. The C. violaceum-induced granuloma requires at least two separate defense pathways, gasdermin D and iNOS, to maintain the integrity of the granuloma architecture. This innate granuloma successfully eradicates C. violaceum infection. Therefore, this C. violaceum-induced granuloma model demonstrates that innate immune cells successfully organize a granuloma and thereby resolve infection by an environmental pathogen.
MeSH term(s)	Animals ; Mice ; Granuloma ; Macrophages/metabolism ; Neutrophils ; Nitric Oxide Synthase Type II/metabolism
Chemical Substances	Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Gsdmd protein, mouse
Language	English
Publishing date	2023-10-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42218-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Neutrophil Caspase-11 Is Essential to Defend against a Cytosol-Invasive Bacterium.

Kovacs, Stephen B / Oh, Changhoon / Maltez, Vivien I / McGlaughon, Benjamin D / Verma, Ambika / Miao, Edward A / Aachoui, Youssef

Cell reports

2020 Volume 32, Issue 4, Page(s) 107967

Abstract: Either caspase-1 or caspase-11 can cleave gasdermin D to cause pyroptosis, eliminating intracellular replication niches. We previously showed that macrophages detect Burkholderia thailandensis via NLRC4, triggering the release of interleukin (IL)-18 and ... ...

Abstract	Either caspase-1 or caspase-11 can cleave gasdermin D to cause pyroptosis, eliminating intracellular replication niches. We previously showed that macrophages detect Burkholderia thailandensis via NLRC4, triggering the release of interleukin (IL)-18 and driving an essential interferon (IFN)-γ response that primes caspase-11. We now identify the IFN-γ-producing cells as a mixture of natural killer (NK) and T cells. Although both caspase-1 and caspase-11 can cleave gasdermin D in macrophages and neutrophils, we find that NLRC4-activated caspase-1 triggers pyroptosis in macrophages, but this pathway does not trigger pyroptosis in neutrophils. In contrast, caspase-11 triggers pyroptosis in both macrophages and neutrophils. This translates to an absolute requirement for caspase-11 in neutrophils during B. thailandensis infection in mice. We present an example of inflammasome sensors causing diverging outcomes in different cell types. Thus, cell fates are dictated not simply by the pathogen or inflammasome, but also by how the cell is wired to respond to detection events.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/metabolism ; Burkholderia/pathogenicity ; Calcium-Binding Proteins/metabolism ; Caspase 1/metabolism ; Caspases/metabolism ; Caspases, Initiator/metabolism ; Cytosol/metabolism ; Female ; Inflammasomes/metabolism ; Interleukin-18/metabolism ; Interleukin-1beta/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Macrophages/metabolism ; Macrophages/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Neutrophils/microbiology ; Phosphate-Binding Proteins/metabolism ; Pyroptosis/immunology ; Pyroptosis/physiology
Chemical Substances	Apoptosis Regulatory Proteins ; Calcium-Binding Proteins ; Gsdmd protein, mouse ; Inflammasomes ; Interleukin-18 ; Interleukin-1beta ; Intracellular Signaling Peptides and Proteins ; Phosphate-Binding Proteins ; Casp4 protein, mouse (EC 3.4.22.-) ; Caspases (EC 3.4.22.-) ; Caspases, Initiator (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
Keywords	covid19
Language	English
Publishing date	2020-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.107967
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Caspase-7 activates ASM to repair gasdermin and perforin pores.

Nozaki, Kengo / Maltez, Vivien I / Rayamajhi, Manira / Tubbs, Alan L / Mitchell, Joseph E / Lacey, Carolyn A / Harvest, Carissa K / Li, Lupeng / Nash, William T / Larson, Heather N / McGlaughon, Benjamin D / Moorman, Nathaniel J / Brown, Michael G / Whitmire, Jason K / Miao, Edward A

Nature

2022 Volume 606, Issue 7916, Page(s) 960–967

Abstract: Among the caspases that cause regulated cell death, a unique function for caspase-7 has remained elusive. Caspase-3 performs apoptosis, whereas caspase-7 is typically considered an inefficient back-up. Caspase-1 activates gasdermin D pores to lyse the ... ...

Abstract	Among the caspases that cause regulated cell death, a unique function for caspase-7 has remained elusive. Caspase-3 performs apoptosis, whereas caspase-7 is typically considered an inefficient back-up. Caspase-1 activates gasdermin D pores to lyse the cell; however, caspase-1 also activates caspase-7 for unknown reasons
MeSH term(s)	Animals ; Apoptosis ; Caspase 7/metabolism ; Chromobacterium/immunology ; Epithelial Cells/cytology ; Intestines/cytology ; Killer Cells, Natural/immunology ; Listeria monocytogenes/immunology ; Mice ; Organoids ; Perforin/metabolism ; Phosphate-Binding Proteins/metabolism ; Pore Forming Cytotoxic Proteins/metabolism ; Sphingomyelin Phosphodiesterase/metabolism ; T-Lymphocytes, Cytotoxic/immunology
Chemical Substances	Gsdmd protein, mouse ; Phosphate-Binding Proteins ; Pore Forming Cytotoxic Proteins ; Perforin (126465-35-8) ; acid sphingomyelinase-1 (EC 3.1.4.-) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12) ; Casp7 protein, mouse (EC 3.4.22.-) ; Caspase 7 (EC 3.4.22.-)
Language	English
Publishing date	2022-06-15
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-04825-8
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Article ; Online: Neutrophil Caspase-11 Is Essential to Defend against a Cytosol-Invasive Bacterium

Stephen B. Kovacs / Changhoon Oh / Vivien I. Maltez / Benjamin D. McGlaughon / Ambika Verma / Edward A. Miao / Youssef Aachoui

Cell Reports, Vol 32, Iss 4, Pp 107967- (2020)

2020

Abstract: Summary: Either caspase-1 or caspase-11 can cleave gasdermin D to cause pyroptosis, eliminating intracellular replication niches. We previously showed that macrophages detect Burkholderia thailandensis via NLRC4, triggering the release of interleukin (IL) ...

Abstract	Summary: Either caspase-1 or caspase-11 can cleave gasdermin D to cause pyroptosis, eliminating intracellular replication niches. We previously showed that macrophages detect Burkholderia thailandensis via NLRC4, triggering the release of interleukin (IL)-18 and driving an essential interferon (IFN)-γ response that primes caspase-11. We now identify the IFN-γ-producing cells as a mixture of natural killer (NK) and T cells. Although both caspase-1 and caspase-11 can cleave gasdermin D in macrophages and neutrophils, we find that NLRC4-activated caspase-1 triggers pyroptosis in macrophages, but this pathway does not trigger pyroptosis in neutrophils. In contrast, caspase-11 triggers pyroptosis in both macrophages and neutrophils. This translates to an absolute requirement for caspase-11 in neutrophils during B. thailandensis infection in mice. We present an example of inflammasome sensors causing diverging outcomes in different cell types. Thus, cell fates are dictated not simply by the pathogen or inflammasome, but also by how the cell is wired to respond to detection events.
Keywords	inflammasome ; pyropotosis ; caspase-1 ; caspase-11 ; NLRC4 ; neutrophil ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2020-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Neutrophil Caspase-11 Is Essential to Defend against a Cytosol-Invasive Bacterium

Kovacs, Stephen B / Oh, Changhoon / Maltez, Vivien I / McGlaughon, Benjamin D / Verma, Ambika / Miao, Edward A / Aachoui, Youssef

Cell Rep

Abstract	Either caspase-1 or caspase-11 can cleave gasdermin D to cause pyroptosis, eliminating intracellular replication niches. We previously showed that macrophages detect Burkholderia thailandensis via NLRC4, triggering the release of interleukin (IL)-18 and driving an essential interferon (IFN)-Î³ response that primes caspase-11. We now identify the IFN-Î³-producing cells as a mixture of natural killer (NK) and T cells. Although both caspase-1 and caspase-11 can cleave gasdermin D in macrophages and neutrophils, we find that NLRC4-activated caspase-1 triggers pyroptosis in macrophages, but this pathway does not trigger pyroptosis in neutrophils. In contrast, caspase-11 triggers pyroptosis in both macrophages and neutrophils. This translates to an absolute requirement for caspase-11 in neutrophils during B. thailandensis infection in mice. We present an example of inflammasome sensors causing diverging outcomes in different cell types. Thus, cell fates are dictated not simply by the pathogen or inflammasome, but also by how the cell is wired to respond to detection events.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #32726630
Database	COVID19

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Article ; Online: Supporting the Next Generation of Scientists to Lead Cancer Immunology Research.

Alspach, Elise / Chow, Ryan D / Demehri, Shadmehr / Guerriero, Jennifer L / Gujar, Shashi / Hartmann, Felix J / Helmink, Beth A / Hudson, William H / Ho, Won Jin / Ma, Leyuan / Maier, Barbara B / Maltez, Vivien I / Miller, Brian C / Moran, Amy E / Parry, Erin M / Pillai, Padmini S / Rafiq, Sarwish / Reina-Campos, Miguel / Rosato, Pamela C /

Rudqvist, Nils-Petter / Ruhland, Megan K / Sagiv-Barfi, Idit / Sahu, Avinash Das / Samstein, Robert M / Schürch, Christian M / Sen, Debattama R / Thommen, Daniela S / Wolf, Yochai / Zappasodi, Roberta

Cancer immunology research

2021 Volume 9, Issue 11, Page(s) 1245–1251

Abstract: Recent success in the use of immunotherapy for a broad range of cancers has propelled the field of cancer immunology to the forefront of cancer research. As more and more young investigators join the community of cancer immunologists, the Arthur L. ... ...

Abstract	Recent success in the use of immunotherapy for a broad range of cancers has propelled the field of cancer immunology to the forefront of cancer research. As more and more young investigators join the community of cancer immunologists, the Arthur L. Irving Family Foundation Cancer Immunology Symposium provided a platform to bring this expanding and vibrant community together and support the development of the future leaders in the field. This commentary outlines the lessons that emerged from the inaugural symposium highlighting the areas of scientific and career development that are essential for professional growth in the field of cancer immunology and beyond. Leading scientists and clinicians in the field provided their experience on the topics of scientific trajectory, career trajectory, publishing, fundraising, leadership, mentoring, and collaboration. Herein, we provide a conceptual and practical framework for career development to the broader scientific community.
MeSH term(s)	Allergy and Immunology/education ; Biomedical Research/methods ; Humans ; Leadership ; Neoplasms/epidemiology ; Physicians/organization & administration
Language	English
Publishing date	2021-09-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-21-0519
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