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Article ; Online: TAK1 inhibition elicits mitochondrial ROS to block intracellular bacterial colonization.

López-Pérez, Wilfred / Sai, Kazuhito / Sakamachi, Yosuke / Parsons, Cameron / Kathariou, Sophia / Ninomiya-Tsuji, Jun

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 25

Abstract: Mitogen-activated protein kinase kinase kinase 7 (MAP3K7), known as TAK1, is an intracellular signaling intermediate of inflammatory responses. However, a series of ... ...

Abstract	Mitogen-activated protein kinase kinase kinase 7 (MAP3K7), known as TAK1, is an intracellular signaling intermediate of inflammatory responses. However, a series of mouse
MeSH term(s)	Animals ; Bacteria/growth & development ; Caspase 3/metabolism ; Colony Count, Microbial ; Hydrogen Sulfide/pharmacology ; Intracellular Space/microbiology ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; MAP Kinase Kinase Kinases/metabolism ; Mice ; Mitochondria/metabolism ; Reactive Oxygen Species/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Salmonella/drug effects ; Salmonella/growth & development ; Yersinia/drug effects
Chemical Substances	Reactive Oxygen Species ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25) ; Caspase 3 (EC 3.4.22.-) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2021-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2023647118
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Article ; Online: Epithelial-derived interleukin-23 promotes oral mucosal immunopathology.

Kim, Tae Sung / Ikeuchi, Tomoko / Theofilou, Vasileios Ionas / Williams, Drake Winslow / Greenwell-Wild, Teresa / June, Armond / Adade, Emmanuel E / Li, Lu / Abusleme, Loreto / Dutzan, Nicolas / Yuan, Yao / Brenchley, Laurie / Bouladoux, Nicolas / Sakamachi, Yosuke / Palmer, Robert J / Iglesias-Bartolome, Ramiro / Trinchieri, Giorgio / Garantziotis, Stavros / Belkaid, Yasmine /

Valm, Alex M / Diaz, Patricia I / Holland, Steven M / Moutsopoulos, Niki M

Immunity

2024 Volume 57, Issue 4, Page(s) 859–875.e11

Abstract: At mucosal surfaces, epithelial cells provide a structural barrier and an immune defense system. However, dysregulated epithelial responses can contribute to disease states. Here, we demonstrated that epithelial cell-intrinsic production of interleukin- ... ...

Abstract	At mucosal surfaces, epithelial cells provide a structural barrier and an immune defense system. However, dysregulated epithelial responses can contribute to disease states. Here, we demonstrated that epithelial cell-intrinsic production of interleukin-23 (IL-23) triggers an inflammatory loop in the prevalent oral disease periodontitis. Epithelial IL-23 expression localized to areas proximal to the disease-associated microbiome and was evident in experimental models and patients with common and genetic forms of disease. Mechanistically, flagellated microbial species of the periodontitis microbiome triggered epithelial IL-23 induction in a TLR5 receptor-dependent manner. Therefore, unlike other Th17-driven diseases, non-hematopoietic-cell-derived IL-23 served as an initiator of pathogenic inflammation in periodontitis. Beyond periodontitis, analysis of publicly available datasets revealed the expression of epithelial IL-23 in settings of infection, malignancy, and autoimmunity, suggesting a broader role for epithelial-intrinsic IL-23 in human disease. Collectively, this work highlights an important role for the barrier epithelium in the induction of IL-23-mediated inflammation.
MeSH term(s)	Humans ; Epithelial Cells ; Inflammation ; Interleukin-23 ; Periodontitis ; Toll-Like Receptor 5/metabolism
Chemical Substances	Interleukin-23 ; Toll-Like Receptor 5
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2024.02.020
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Zs.A 4227: 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)
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Article ; Online: Erratum: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1.

Mihaly, September R / Sakamachi, Yosuke / Ninomiya-Tsuji, Jun / Morioka, Sho

Scientific reports

2017 Volume 7, Issue 1, Page(s) 10695

Abstract: A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper. ...

Abstract	A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper.
Language	English
Publishing date	2017-09-06
Publishing country	England
Document type	Journal Article ; Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-09609-z
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Article ; Online: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1.

Mihaly, September R / Sakamachi, Yosuke / Ninomiya-Tsuji, Jun / Morioka, Sho

Scientific reports

2017 Volume 7, Issue 1, Page(s) 2918

Abstract: Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of cell ... ...

Abstract	Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of cell death is crucial for tissue homeostasis. Indeed, necroptosis is triggered by caspase inhibition to ensure cell death. Here we identified a previously uncharacterized cell death pathway regulated by TAK1, which is unexpectedly provoked by inhibition of caspase activity and necroptosis cascades. Ablation of TAK1 triggers spontaneous death in macrophages. Simultaneous inhibition of caspases and RIPK3 did not completely restore cell viability. Previous studies demonstrated that loss of TAK1 in fibroblasts causes TNF-induced apoptosis and that additional inhibition of caspase leads to necroptotic cell death. However, we surprisingly found that caspase and RIPK3 inhibitions do not completely suppress cell death in Tak1-deficient cells. Mechanistically, the execution of the third cell death pathway in Tak1-deficient macrophages and fibroblasts were mediated by RIPK1-dependent rapid accumulation of reactive oxygen species (ROS). Conversely, activation of RIPK1 was sufficient to induce cell death. Therefore, loss of TAK1 elicits noncanonical cell death which is mediated by RIPK1-induced oxidative stress upon caspase and necroptosis inhibition to further ensure induction of cell death.
Language	English
Publishing date	2017-06-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-03112-1
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Article ; Online: Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1

September R. Mihaly / Yosuke Sakamachi / Jun Ninomiya-Tsuji / Sho Morioka

Scientific Reports, Vol 7, Iss 1, Pp 1-

2017 Volume 12

Abstract: Abstract Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of ...

Abstract	Abstract Programmed cell death (PCD) occurs in several forms including apoptosis and necroptosis. Apoptosis is executed by the activation of caspases, while necroptosis is dependent on the receptor interacting protein kinase 3 (RIPK3). Precise control of cell death is crucial for tissue homeostasis. Indeed, necroptosis is triggered by caspase inhibition to ensure cell death. Here we identified a previously uncharacterized cell death pathway regulated by TAK1, which is unexpectedly provoked by inhibition of caspase activity and necroptosis cascades. Ablation of TAK1 triggers spontaneous death in macrophages. Simultaneous inhibition of caspases and RIPK3 did not completely restore cell viability. Previous studies demonstrated that loss of TAK1 in fibroblasts causes TNF-induced apoptosis and that additional inhibition of caspase leads to necroptotic cell death. However, we surprisingly found that caspase and RIPK3 inhibitions do not completely suppress cell death in Tak1-deficient cells. Mechanistically, the execution of the third cell death pathway in Tak1-deficient macrophages and fibroblasts were mediated by RIPK1-dependent rapid accumulation of reactive oxygen species (ROS). Conversely, activation of RIPK1 was sufficient to induce cell death. Therefore, loss of TAK1 elicits noncanonical cell death which is mediated by RIPK1-induced oxidative stress upon caspase and necroptosis inhibition to further ensure induction of cell death.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2017-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: TAK1 regulates resident macrophages by protecting lysosomal integrity.

Sakamachi, Yosuke / Morioka, Sho / Mihaly, September R / Takaesu, Giichi / Foley, Julie F / Fessler, Michael B / Ninomiya-Tsuji, Jun

Cell death & disease

2017 Volume 8, Issue 2, Page(s) e2598

Abstract: Hematopoietic cell survival and death is critical for development of a functional immune system. Here, we report that a protein kinase, TAK1, is selectively required for resident macrophage integrity during embryogenesis. Hematopoietic lineage-specific ... ...

Abstract	Hematopoietic cell survival and death is critical for development of a functional immune system. Here, we report that a protein kinase, TAK1, is selectively required for resident macrophage integrity during embryogenesis. Hematopoietic lineage-specific deletion of Tak1 gene (Tak1
MeSH term(s)	Animals ; Cell Death/physiology ; Cell Survival/physiology ; Embryonic Development/physiology ; Lung/metabolism ; Lysosomes/metabolism ; MAP Kinase Kinase Kinases/metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Protective Agents/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Signal Transduction/physiology ; Thymocytes/physiology ; Thymus Gland/metabolism ; Toll-Like Receptors/metabolism
Chemical Substances	Protective Agents ; Receptors, Tumor Necrosis Factor, Type I ; Toll-Like Receptors ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP kinase kinase kinase 7 (EC 2.7.11.25)
Language	English
Publishing date	2017-02-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2017.23
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Article ; Online: TLR5 participates in the TLR4 receptor complex and promotes MyD88-dependent signaling in environmental lung injury.

eLife

2020 Volume 9

Abstract: Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone ( ... ...

Abstract	Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone (O
MeSH term(s)	Animals ; Cells, Cultured ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Lung/immunology ; Lung/metabolism ; Lung Injury/chemically induced ; Lung Injury/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Polymorphism, Single Nucleotide/genetics ; Signal Transduction/genetics ; Signal Transduction/immunology ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism ; Toll-Like Receptor 5/genetics ; Toll-Like Receptor 5/metabolism
Chemical Substances	MYD88 protein, human ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; TLR4 protein, human ; TLR5 protein, human ; Tlr4 protein, mouse ; Tlr5 protein, mouse ; Toll-Like Receptor 4 ; Toll-Like Receptor 5
Language	English
Publishing date	2020-01-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.50458
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Article ; Online: Therapeutic responses to

Myles, Ian A / Castillo, Carlo R / Barbian, Kent D / Kanakabandi, Kishore / Virtaneva, Kimmo / Fitzmeyer, Emily / Paneru, Monica / Otaizo-Carrasquero, Francisco / Myers, Timothy G / Markowitz, Tovah E / Moore, Ian N / Liu, Xue / Ferrer, Marc / Sakamachi, Yosuke / Garantziotis, Stavros / Swamydas, Muthulekha / Lionakis, Michail S / Anderson, Erik D / Earland, Noah J /

Ganesan, Sundar / Sun, Ashleigh A / Bergerson, Jenna R E / Silverman, Robert A / Petersen, Maureen / Martens, Craig A / Datta, Sandip K

Science translational medicine

2020 Volume 12, Issue 560

Abstract: Dysbiosis of the skin microbiota is increasingly implicated as a contributor to the pathogenesis of atopic dermatitis (AD). We previously reported first-in-human safety and clinical activity results from topical application of the commensal skin ... ...

Abstract	Dysbiosis of the skin microbiota is increasingly implicated as a contributor to the pathogenesis of atopic dermatitis (AD). We previously reported first-in-human safety and clinical activity results from topical application of the commensal skin bacterium
MeSH term(s)	Adult ; Child ; Dermatitis, Atopic/drug therapy ; Eczema ; Humans ; Lipids ; Methylobacteriaceae ; Skin
Chemical Substances	Lipids
Language	English
Publishing date	2020-09-09
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Intramural
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.aaz8631
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Article ; Online: TLR5 participates in the TLR4 receptor complex and promotes MyD88-dependent signaling in environmental lung injury

eLife, Vol

2020 Volume 9

Abstract: Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone (O3). Toll-like receptors (TLRs) orchestrate immune responses to injury by recognizing pathogen- or ...

Abstract	Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone (O3). Toll-like receptors (TLRs) orchestrate immune responses to injury by recognizing pathogen- or danger-associated molecular patterns. TLR4, the prototypic receptor for LPS, also mediates inflammation after O3, triggered by endogenous hyaluronan. Regulation of TLR4 signaling is incompletely understood. TLR5, the flagellin receptor, is expressed in alveolar macrophages, and regulates immune responses to environmental injury. Using in vivo animal models of TLR4-mediated inflammations (LPS, O3, hyaluronan), we show that TLR5 impacts the in vivo response to LPS, hyaluronan and O3. We demonstrate that immune cells of human carriers of a dominant negative TLR5 allele have decreased inflammatory response to O3 exposure ex vivo and LPS exposure in vitro. Using primary murine macrophages, we find that TLR5 physically associates with TLR4 and biases TLR4 signaling towards the MyD88 pathway. Our results suggest an updated paradigm for TLR4/TLR5 signaling.
Keywords	inflammation ; innate immune receptors ; TLR4 ; TLR5 ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Wastewater Remediation Using Algae Grown on a Substrate for Biomass and Biofuel Production

James B. Houser / Mark E. Venable / Yosuke Sakamachi / Michael S. Hambourger / Jacob Herrin / Shea R. Tuberty

Journal of Environmental Protection , Vol 05, Iss 10, Pp 895-

2014 Volume 904

Abstract: Surging oil, feed and fertilizer costs have impacted farmers particularly hard. Farm-based, local sources of renewable energy could help reduce energy costs for farmers and help develop rural-based processing and manufacturing of biofuel to bolster rural ...

Abstract	Surging oil, feed and fertilizer costs have impacted farmers particularly hard. Farm-based, local sources of renewable energy could help reduce energy costs for farmers and help develop rural-based processing and manufacturing of biofuel to bolster rural economies. At the same time, nutrient contamination and eutrophication from farming operations have become national problems. Algal-based bioprocessors have the potential to address these problems simultaneously. At Appalachian State University (Appstate) we set out to design, build and test a system that uses algae to capture wastewater nutrients as well as excreted pharmaceuticals, while simultaneously sequestering CO 2 , producing oil for conversion to biodiesel and feed for livestock. There are a number of problems with current algae growth systems. Algae grown in an open pond or raceway system are suspended in the water in the presence of soluble and suspended waste making most of the current harvest techniques problematic and expensive. Appstate designed algae troughs in which the algae are immobilized on a solid substrate. The laboratory-scale prototype was constructed of three-sided square plastic pipe open at the top. Inside the pipe, there was a series of cloth filters supported by rigid flow-through baffles. Preliminary results observed an average percent reduction of nitrate and phosphorous of 40 and 43, respectively, from different initial nutrient concentrations. Near complete removal (~96%) of estrogen was observed in 2-day trial experiments. In addition, effective increases in algal biomass which can serve as both biofuel feedstock and livestock feed were observed.
Keywords	Algae ; Wastewater Remediation ; CAFO ; Eutrophication ; Biomass Production ; Biofuels ; Environmental sciences ; GE1-350 ; Geography. Anthropology. Recreation ; G
Subject code	571
Language	English
Publishing date	2014-07-01T00:00:00Z
Publisher	Scientific Research Publishing
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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