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  1. Article ; Online: Phagocyte NADPH oxidase, chronic granulomatous disease and mycobacterial infections.

    Deffert, Christine / Cachat, Julien / Krause, Karl-Heinz

    Cellular microbiology

    2014  Volume 16, Issue 8, Page(s) 1168–1178

    Abstract: Infection of humans with Mycobacterium tuberculosis remains frequent and may still lead to death. After primary infection, the immune system is often able to control M. tuberculosis infection over a prolonged latency period, but a decrease in immune ... ...

    Abstract Infection of humans with Mycobacterium tuberculosis remains frequent and may still lead to death. After primary infection, the immune system is often able to control M. tuberculosis infection over a prolonged latency period, but a decrease in immune function (from HIV to immunosenescence) leads to active disease. Available vaccines against tuberculosis are restricted to BCG, a live vaccine with an attenuated strain of M. bovis. Immunodeficiency may not only be associated with an increased risk of tuberculosis, but also with local or disseminated BCG infection. Genetic deficiency in the reactive oxygen species (ROS)-producing phagocyte NADPH oxidase NOX2 is called chronic granulomatous disease (CGD). CGD is among the most common primary immune deficiencies. Here we review our knowledge on the importance of NOX2-derived ROS in mycobacterial infection. A literature review suggests that human CGD patient frequently have an increased susceptibility to BCG and to M. tuberculosis. In vitro studies and experiments with CGD mice are incomplete and yielded - at least in part - contradictory results. Thus, although observations in human CGD patients leave little doubt about the role of NOX2 in the control of mycobacteria, further studies will be necessary to unequivocally define and understand the role of ROS.
    MeSH term(s) Animals ; Apoptosis/immunology ; Extracellular Traps/immunology ; Granulomatous Disease, Chronic/immunology ; Humans ; Membrane Glycoproteins/immunology ; Mice ; Mycobacterium Infections/immunology ; Mycobacterium bovis/immunology ; Mycobacterium tuberculosis/immunology ; Mycobacterium tuberculosis/pathogenicity ; NADPH Oxidase 2 ; NADPH Oxidases/immunology ; Phagocytosis/immunology ; Phagosomes/immunology ; Reactive Oxygen Species/immunology ; Tuberculosis, Pulmonary/immunology ; Tuberculosis, Pulmonary/pathology ; Tuberculosis, Pulmonary/prevention & control
    Chemical Substances Membrane Glycoproteins ; Reactive Oxygen Species ; CYBB protein, human (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2014-08
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1468320-9
    ISSN 1462-5822 ; 1462-5814
    ISSN (online) 1462-5822
    ISSN 1462-5814
    DOI 10.1111/cmi.12322
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Phagocyte NADPH oxidase and specific immunity.

    Cachat, Julien / Deffert, Christine / Hugues, Stephanie / Krause, Karl-Heinz

    Clinical science (London, England : 1979)

    2015  Volume 128, Issue 10, Page(s) 635–648

    Abstract: The phagocyte NADPH oxidase NOX2 produces reactive oxygen species (ROS) and is a well-known player in host defence. However, there is also increasing evidence for a regulatory role of NOX2 in adaptive immunity. Deficiency in phagocyte NADPH oxidase ... ...

    Abstract The phagocyte NADPH oxidase NOX2 produces reactive oxygen species (ROS) and is a well-known player in host defence. However, there is also increasing evidence for a regulatory role of NOX2 in adaptive immunity. Deficiency in phagocyte NADPH oxidase causes chronic granulomatous disease (CGD) in humans, a condition that can also be studied in CGD mice. Clinical observations in CGD patients suggest a higher susceptibility to autoimmune diseases, in particular lupus, idiopathic thrombocytopenic purpura and rheumatoid arthritis. In mice, a strong correlation exists between a polymorphism in a NOX2 subunit and the development of autoimmune arthritis. NOX2 deficiency in mice also favours lupus development. Both CGD patients and CGD mice exhibit increased levels of immunoglobulins, including autoantibodies. Despite these phenotypes suggesting a role for NOX2 in specific immunity, mechanistic explanations for the typical increase of CGD in autoimmune disease and antibody levels are still preliminary. NOX2-dependent ROS generation is well documented for dendritic cells and B-lymphocytes. It is unclear whether T-lymphocytes produce ROS themselves or whether they are exposed to ROS derived from dendritic cells during the process of antigen presentation. ROS are signalling molecules in virtually any cell type, including T- and B-lymphocytes. However, knowledge about the impact of ROS-dependent signalling on T- and B-lymphocyte phenotype and response is still limited. ROS might contribute to Th1/Th2/Th17 cell fate decisions during T-lymphocyte activation and might enhance immunoglobulin production by B-lymphocytes. In dendritic cells, NOX2-derived ROS might be important for antigen processing and cell activation.
    MeSH term(s) Adaptive Immunity/immunology ; Animals ; Granulomatous Disease, Chronic/immunology ; Granulomatous Disease, Chronic/metabolism ; Humans ; Immunity, Innate/immunology ; Lymphocytes/cytology ; Lymphocytes/metabolism ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/immunology ; Mice ; Myelin-Oligodendrocyte Glycoprotein/immunology ; NADPH Oxidase 2 ; NADPH Oxidases/deficiency ; NADPH Oxidases/immunology ; Phagocytes/enzymology ; Phagocytes/immunology ; Reactive Oxygen Species/metabolism ; Signal Transduction/immunology
    Chemical Substances MOG protein, human ; Membrane Glycoproteins ; Myelin-Oligodendrocyte Glycoprotein ; Reactive Oxygen Species ; CYBB protein, human (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2015-05-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20140635
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  3. Article: Altered Humoral Immune Responses and IgG Subtypes in NOX2-Deficient Mice and Patients: A Key Role for NOX2 in Antigen-Presenting Cells.

    Cachat, Julien / Deffert, Christine / Alessandrini, Marco / Roux-Lombard, Pascale / Le Gouellec, Audrey / Stasia, Marie-José / Hugues, Stéphanie / Krause, Karl-Heinz

    Frontiers in immunology

    2018  Volume 9, Page(s) 1555

    Abstract: Chronic granulomatous disease (CGD) is a primary immunodeficiency resulting from loss of function mutations in the reactive oxygen species generating phagocyte NADPH oxidase (NOX2). CGD patients are prone to infection, but also have an increased ... ...

    Abstract Chronic granulomatous disease (CGD) is a primary immunodeficiency resulting from loss of function mutations in the reactive oxygen species generating phagocyte NADPH oxidase (NOX2). CGD patients are prone to infection, but also have an increased susceptibility to autoimmune diseases. The aim of this study was to investigate the role of NOX2 in the regulation of specific immunity. In both CGD patients and NOX2-deficient mice, we observed an alteration in the basal proportions of IgG subtypes. Upon immunization with curdlan-a dectin 1 agonist-NOX2-deficient mice showed increased production of IgG2c compared to controls, and restimulation of lymph node-derived cells led to increased production of IFNγ, but not IL-5, indicative hallmark of an enhanced Th1 response. T cell activation was increased in NOX2-deficient mice and a similar trend was observed
    Language English
    Publishing date 2018
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.01555
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  4. Article ; Online: Bacillus calmette-guerin infection in NADPH oxidase deficiency: defective mycobacterial sequestration and granuloma formation.

    Deffert, Christine / Schäppi, Michela G / Pache, Jean-Claude / Cachat, Julien / Vesin, Dominique / Bisig, Ruth / Ma Mulone, Xiaojuan / Kelkka, Tiina / Holmdahl, Rikard / Garcia, Irene / Olleros, Maria L / Krause, Karl-Heinz

    PLoS pathogens

    2014  Volume 10, Issue 9, Page(s) e1004325

    Abstract: Patients with chronic granulomatous disease (CGD) lack generation of reactive oxygen species (ROS) through the phagocyte NADPH oxidase NOX2. CGD is an immune deficiency that leads to frequent infections with certain pathogens; this is well documented for ...

    Abstract Patients with chronic granulomatous disease (CGD) lack generation of reactive oxygen species (ROS) through the phagocyte NADPH oxidase NOX2. CGD is an immune deficiency that leads to frequent infections with certain pathogens; this is well documented for S. aureus and A. fumigatus, but less clear for mycobacteria. We therefore performed an extensive literature search which yielded 297 cases of CGD patients with mycobacterial infections; M. bovis BCG was most commonly described (74%). The relationship between NOX2 deficiency and BCG infection however has never been studied in a mouse model. We therefore investigated BCG infection in three different mouse models of CGD: Ncf1 mutants in two different genetic backgrounds and Cybb knock-out mice. In addition, we investigated a macrophage-specific rescue (transgenic expression of Ncf1 under the control of the CD68 promoter). Wild-type mice did not develop severe disease upon BCG injection. In contrast, all three types of CGD mice were highly susceptible to BCG, as witnessed by a severe weight loss, development of hemorrhagic pneumonia, and a high mortality (∼ 50%). Rescue of NOX2 activity in macrophages restored BCG resistance, similar as seen in wild-type mice. Granulomas from mycobacteria-infected wild-type mice generated ROS, while granulomas from CGD mice did not. Bacterial load in CGD mice was only moderately increased, suggesting that it was not crucial for the observed phenotype. CGD mice responded with massively enhanced cytokine release (TNF-α, IFN-γ, IL-17 and IL-12) early after BCG infection, which might account for severity of the disease. Finally, in wild-type mice, macrophages formed clusters and restricted mycobacteria to granulomas, while macrophages and mycobacteria were diffusely distributed in lung tissue from CGD mice. Our results demonstrate that lack of the NADPH oxidase leads to a markedly increased severity of BCG infection through mechanisms including increased cytokine production and impaired granuloma formation.
    MeSH term(s) Animals ; Cytokines/metabolism ; Female ; Granuloma/immunology ; Granuloma/pathology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mycobacterium Infections/immunology ; Mycobacterium Infections/microbiology ; Mycobacterium Infections/pathology ; Mycobacterium bovis/pathogenicity ; NADPH Oxidases/physiology ; Nitric Oxide Synthase Type II/metabolism ; Reactive Oxygen Species/metabolism ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism
    Chemical Substances Cytokines ; Reactive Oxygen Species ; 3-nitrotyrosine (3604-79-3) ; Tyrosine (42HK56048U) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2014-09-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1004325
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  5. Article ; Online: Macrophage-specific NOX2 contributes to the development of lung emphysema through modulation of SIRT1/MMP-9 pathways.

    Trocme, Candice / Deffert, Christine / Cachat, Julien / Donati, Yves / Tissot, Christelle / Papacatzis, Sylvie / Braunersreuther, Vincent / Pache, Jean-Claude / Krause, Karl-Heinz / Holmdahl, Rikard / Barazzone-Argiroffo, Constance / Carnesecchi, Stéphanie

    The Journal of pathology

    2014  Volume 235, Issue 1, Page(s) 65–78

    Abstract: Reactive oxygen species (ROS) participate in the pathogenesis of emphysema. Among ROS-producing enzymes, NOX NADPH oxidases are thought to be responsible for tissue injury associated with several lung pathologies. To determine whether NOX2 and/or NOX1 ... ...

    Abstract Reactive oxygen species (ROS) participate in the pathogenesis of emphysema. Among ROS-producing enzymes, NOX NADPH oxidases are thought to be responsible for tissue injury associated with several lung pathologies. To determine whether NOX2 and/or NOX1 participate in the development of emphysema, their expression patterns were first studied by immunohistochemistry in the lungs of emphysematous patients. Subsequently, we investigated their contribution to elastase-induced emphysema using NOX2- and NOX1-deficient mice. In human lung, NOX2 was mainly detected in macrophages of control and emphysematous lungs, while NOX1 was expressed in alveolar epithelium and bronchial cells. We observed an elevated number of NOX2-positive cells in human emphysematous lungs, as well as increased NOX2 and NOX1 mRNA expression in mouse lungs following elastase exposure. Elastase-induced alveolar airspace enlargement and elastin degradation were prevented in NOX2-deficient mice, but not in NOX1-deficient mice. This protection was independent of inflammation and correlated with reduced ROS production. Concomitantly, an elevation of sirtuin 1 (SIRT1) level and a decrease of matrix metalloproteinase-9 (MMP-9) expression and activity were observed in alveolar macrophages and neutrophils. We addressed the specific role of macrophage-restricted functional NOX2 in elastase-induced lung emphysema using Ncf1 mutant mice and Ncf1 macrophage rescue mice (Ncf1 mutant mice with transgenic expression of Ncf1 only in CD68-positive mononuclear phagocytes; the MN mouse). Compared to WT mice, the lack of functional NOX2 led to decreased elastase-induced ROS production and protected against emphysema. In contrast, ROS production was restored specifically in macrophages from Ncf1 rescue mice and contributes to emphysema. Taken together, our results demonstrate that NOX2 is involved in the pathogenesis of human emphysema and macrophage-specific NOX2 participates in elastase-induced emphysema through the involvement of SIRT1/MMP-9 pathways in mice.
    MeSH term(s) Animals ; Humans ; Inflammation/pathology ; Lung/pathology ; Macrophages/metabolism ; Macrophages/pathology ; Matrix Metalloproteinase 9/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; NADPH Oxidase 2 ; NADPH Oxidases/metabolism ; Neutrophils/pathology ; Pulmonary Emphysema/metabolism ; Pulmonary Emphysema/pathology ; Reactive Oxygen Species/metabolism ; Sirtuin 1/metabolism
    Chemical Substances Membrane Glycoproteins ; Reactive Oxygen Species ; CYBB protein, human (EC 1.6.3.-) ; Cybb protein, mouse (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; MMP9 protein, human (EC 3.4.24.35) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35) ; Sirtuin 1 (EC 3.5.1.-)
    Language English
    Publishing date 2014-11-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.4423
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  6. Article ; Online: C-terminal tensin-like gene functions as an oncogene and promotes cell motility in pancreatic cancer.

    Al-Ghamdi, Saleh / Cachat, Julien / Albasri, Abdulkader / Ahmed, Mohammed / Jackson, Darryl / Zaitoun, Abed / Guppy, Naomi / Otto, William R / Alison, Malcolm R / Kindle, Karin B / Ilyas, Mohammad

    Pancreas

    2013  Volume 42, Issue 1, Page(s) 135–140

    Abstract: Objectives: C-terminal tensin-like gene (CTEN, also known as TNS4) localizes to focal adhesions and is reported to function as an oncogene in colonic, breast, lung, and gastric cancers. Its role in pancreatic cancer is unknown and was thus investigated ... ...

    Abstract Objectives: C-terminal tensin-like gene (CTEN, also known as TNS4) localizes to focal adhesions and is reported to function as an oncogene in colonic, breast, lung, and gastric cancers. Its role in pancreatic cancer is unknown and was thus investigated in this study.
    Methods: C-terminal tensinlike gene expression was evaluated by immunohistochemistry in a series of pancreatic cancers. Functional activity of the CTEN was tested by manipulating cellular CTEN levels using a dual approach of gene knockdown/forced expression.
    Results: The CTEN is overexpressed in 31 (70.45%) of 44 pancreatic cancers. Functionally, changes in CTEN level did not alter cellular proliferation, but CTEN levels were positively associated with enhanced colony-forming efficiency in both Panc-1 and PSN-1 cell lines. Forced CTEN expression in Panc-1 cells stimulated cell motility, whereas knockdown of CTEN in PSN-1 inhibited cell motility in both transwell migration and wound-healing assays. Evaluation of downstream targets demonstrated that alterations in CTEN levels induced changes in focal adhesion kinase and E-cadherin, whereas integrin-linked kinase (ILK) remained unchanged.
    Conclusions: These are the first data showing an oncogenic role for CTEN in pancreatic cancer through promotion of colony formation and cell motility. The latter may be mediated by signaling through focal adhesion kinase and inhibiting E-cadherin.
    MeSH term(s) Cadherins/metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Focal Adhesion Kinase 1/metabolism ; Gene Knockdown Techniques ; Humans ; Immunohistochemistry ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Neoplasm Invasiveness ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Protein-Serine-Threonine Kinases/metabolism ; RNA Interference ; Signal Transduction ; Tensins ; Time Factors ; Tissue Array Analysis ; Transfection ; Up-Regulation
    Chemical Substances CDH1 protein, human ; Cadherins ; Microfilament Proteins ; Oncogene Proteins ; TNS4 protein, human ; Tensins ; integrin-linked kinase (EC 2.7.1.-) ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; PTK2 protein, human (EC 2.7.10.2) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2013-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632831-3
    ISSN 1536-4828 ; 0885-3177
    ISSN (online) 1536-4828
    ISSN 0885-3177
    DOI 10.1097/MPA.0b013e3182557ceb
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  7. Article ; Online: Cten is targeted by Kras signalling to regulate cell motility in the colon and pancreas.

    Al-Ghamdi, Saleh / Albasri, Abdulkader / Cachat, Julien / Ibrahem, Salih / Muhammad, Belal A / Jackson, Darryl / Nateri, Abdolrahman S / Kindle, Karin B / Ilyas, Mohammad

    PloS one

    2011  Volume 6, Issue 6, Page(s) e20919

    Abstract: CTEN/TNS4 is an oncogene in colorectal cancer (CRC) which enhances cell motility although the mechanism of Cten regulation is unknown. We found an association between high Cten expression and KRAS/BRAF mutation in a series of CRC cell lines (p = 0.03) ... ...

    Abstract CTEN/TNS4 is an oncogene in colorectal cancer (CRC) which enhances cell motility although the mechanism of Cten regulation is unknown. We found an association between high Cten expression and KRAS/BRAF mutation in a series of CRC cell lines (p = 0.03) and hypothesised that Kras may regulate Cten. To test this, Kras was knocked-down (using small interfering (si)RNA) in CRC cell lines SW620 and DLD1 (high Cten expressors and mutant for KRAS). In each cell line, Kras knockdown was mirrored by down-regulation of Cten Since Kras signals through Braf, we tested the effect of Kras knockdown in CRC cell line Colo205 (which shows high Cten expression and is mutant for BRAF but wild type for KRAS). Cten levels were unaffected by Kras knockdown whilst Braf knockdown resulted in reduced Cten expression suggesting that Kras signals via Braf to regulate Cten. Quantification of Cten mRNA and protein analysis following proteasome inhibition suggested that regulation was of Cten transcription. Kras knockdown inhibited cell motility. To test whether this could be mediated through Cten, SW620 cells were co-transfected with Kras specific siRNAs and a Cten expression vector. Restoring Cten expression was able to restore cell motility despite Kras knockdown (transwell migration and wounding assay, p<0.001 for both). Since KRAS is mutated in many cancers, we investigated whether this relationship could be demonstrated in other tumour models. The experiments were repeated in the pancreatic cancer cell lines Colo357 & PSN-1(both high Cten expressors and mutant for KRAS). In both cell lines, Kras was shown to regulate Cten and forced expression of Cten was able to rescue loss of cell motility following Kras knockdown in PSN-1 (transwell migration assay, p<0.001). We conclude that, in the colon and pancreas, Cten is a downstream target of Kras and may be a mechanism through which Kras regulates of cell motility.
    MeSH term(s) Base Sequence ; Cell Line, Tumor ; Cell Movement ; Colon/cytology ; Colon/metabolism ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/pathology ; Flow Cytometry ; Gene Knockdown Techniques ; Genes, ras ; Humans ; Microfilament Proteins/metabolism ; Pancreas/cytology ; Pancreas/metabolism ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; RNA, Small Interfering ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tensins
    Chemical Substances Microfilament Proteins ; RNA, Small Interfering ; TNS4 protein, human ; Tensins
    Language English
    Publishing date 2011-06-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0020919
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  8. Article ; Online: Innate immunity. A Spaetzle-like role for nerve growth factor β in vertebrate immunity to Staphylococcus aureus.

    Hepburn, Lucy / Prajsnar, Tomasz K / Klapholz, Catherine / Moreno, Pablo / Loynes, Catherine A / Ogryzko, Nikolay V / Brown, Karen / Schiebler, Mark / Hegyi, Krisztina / Antrobus, Robin / Hammond, Katherine L / Connolly, John / Ochoa, Bernardo / Bryant, Clare / Otto, Michael / Surewaard, Bas / Seneviratne, Suranjith L / Grogono, Dorothy M / Cachat, Julien /
    Ny, Tor / Kaser, Arthur / Török, M Estée / Peacock, Sharon J / Holden, Matthew / Blundell, Tom / Wang, Lihui / Ligoxygakis, Petros / Minichiello, Liliana / Woods, C Geoff / Foster, Simon J / Renshaw, Stephen A / Floto, R Andres

    Science (New York, N.Y.)

    2014  Volume 346, Issue 6209, Page(s) 641–646

    Abstract: Many key components of innate immunity to infection are shared between Drosophila and humans. However, the fly Toll ligand Spaetzle is not thought to have a vertebrate equivalent. We have found that the structurally related cystine-knot protein, nerve ... ...

    Abstract Many key components of innate immunity to infection are shared between Drosophila and humans. However, the fly Toll ligand Spaetzle is not thought to have a vertebrate equivalent. We have found that the structurally related cystine-knot protein, nerve growth factor β (NGFβ), plays an unexpected Spaetzle-like role in immunity to Staphylococcus aureus infection in chordates. Deleterious mutations of either human NGFβ or its high-affinity receptor tropomyosin-related kinase receptor A (TRKA) were associated with severe S. aureus infections. NGFβ was released by macrophages in response to S. aureus exoproteins through activation of the NOD-like receptors NLRP3 and NLRP4 and enhanced phagocytosis and superoxide-dependent killing, stimulated proinflammatory cytokine production, and promoted calcium-dependent neutrophil recruitment. TrkA knockdown in zebrafish increased susceptibility to S. aureus infection, confirming an evolutionarily conserved role for NGFβ-TRKA signaling in pathogen-specific host immunity.
    MeSH term(s) Animals ; Drosophila melanogaster/genetics ; Drosophila melanogaster/immunology ; Evolution, Molecular ; Gene Knockdown Techniques ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Humans ; Macrophages/immunology ; Nerve Growth Factor/genetics ; Nerve Growth Factor/immunology ; Phagocytosis/genetics ; Phagocytosis/immunology ; Receptor, trkA/genetics ; Receptor, trkA/immunology ; Staphylococcal Infections/genetics ; Staphylococcal Infections/immunology ; Staphylococcus aureus/immunology ; Zebrafish/genetics ; Zebrafish/immunology
    Chemical Substances Nerve Growth Factor (9061-61-4) ; Receptor, trkA (EC 2.7.10.1)
    Language English
    Publishing date 2014-10-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1258705
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