دورية أكاديمية
Targeting NLRP3 and Staphylococcal pore-forming toxin receptors in human-induced pluripotent stem cell-derived macrophages.
| العنوان: | Targeting NLRP3 and Staphylococcal pore-forming toxin receptors in human-induced pluripotent stem cell-derived macrophages. |
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| المؤلفون: | Chow SH; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Deo P; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Yeung ATY; The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK., Kostoulias XP; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia., Jeon Y; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Gao ML; Laboratory of Stem Cell & Retinal Regeneration, Institute of Stem Cell Research, Division of Ophthalmic Genetics, The Eye Hospital, Wenzhou Medical University, Wenzhou, China.; National Center for International Research in Regenerative Medicine and Neurogenetics, National Clinical Research Center for Ophthalmology, State Key Laboratory of Ophthalmology, Optometry and Visual Science, Wenzhou, China., Seidi A; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Olivier FAB; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Sridhar S; The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK., Nethercott C; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia., Cameron D; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia., Robertson AAB; School of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia, Queensland, Australia., Robert R; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Mackay CR; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia., Traven A; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia., Jin ZB; Laboratory of Stem Cell & Retinal Regeneration, Institute of Stem Cell Research, Division of Ophthalmic Genetics, The Eye Hospital, Wenzhou Medical University, Wenzhou, China.; National Center for International Research in Regenerative Medicine and Neurogenetics, National Clinical Research Center for Ophthalmology, State Key Laboratory of Ophthalmology, Optometry and Visual Science, Wenzhou, China., Hale C; The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK., Dougan G; The Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK.; Department of Medicine, Addenbrookes Hospital, Cambridge, UK., Peleg AY; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia.; Department of Infectious Diseases, the Alfred Hospital and Central Clinical School, Monash University, Melbourne, Australia., Naderer T; Infection & Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, Australia. |
| المصدر: | Journal of leukocyte biology [J Leukoc Biol] 2020 Sep; Vol. 108 (3), pp. 967-981. Date of Electronic Publication: 2020 Jun 12. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Oxford University Press Country of Publication: England NLM ID: 8405628 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1938-3673 (Electronic) Linking ISSN: 07415400 NLM ISO Abbreviation: J Leukoc Biol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2023- : Oxford : Oxford University Press Original Publication: New York : Alan R. Liss, c1984- |
| مواضيع طبية MeSH: | Staphylococcus aureus*/physiology, Bacterial Proteins/*antagonists & inhibitors , Bacterial Toxins/*antagonists & inhibitors , Exotoxins/*antagonists & inhibitors , Induced Pluripotent Stem Cells/*cytology , Leukocidins/*antagonists & inhibitors , Macrophages/*drug effects , NLR Family, Pyrin Domain-Containing 3 Protein/*antagonists & inhibitors , Receptor, Anaphylatoxin C5a/*drug effects, Animals ; CD11b Antigen/immunology ; CRISPR-Cas Systems ; Cell Differentiation ; Cells, Cultured ; Exotoxins/deficiency ; Gene Knock-In Techniques ; Humans ; Interleukin-1beta/metabolism ; Leukocyte Common Antigens/physiology ; Lung/immunology ; Lung/microbiology ; Macrophages/cytology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology ; Peptide Fragments/immunology ; Pneumonia, Staphylococcal/immunology ; Protein Subunits ; Receptor, Anaphylatoxin C5a/deficiency ; Receptor, Anaphylatoxin C5a/genetics ; Receptor, Anaphylatoxin C5a/physiology ; Recombinant Proteins/metabolism |
| مستخلص: | Staphylococcus aureus causes necrotizing pneumonia by secreting toxins such as leukocidins that target front-line immune cells. The mechanism by which leukocidins kill innate immune cells and trigger inflammation during S. aureus lung infection, however, remains unresolved. Here, we explored human-induced pluripotent stem cell-derived macrophages (hiPSC-dMs) to study the interaction of the leukocidins Panton-Valentine leukocidin (PVL) and LukAB with lung macrophages, which are the initial leukocidin targets during S. aureus lung invasion. hiPSC-dMs were susceptible to the leukocidins PVL and LukAB and both leukocidins triggered NLPR3 inflammasome activation resulting in IL-1β secretion. hiPSC-dM cell death after LukAB exposure, however, was only temporarily dependent of NLRP3, although NLRP3 triggered marked cell death after PVL treatment. CRISPR/Cas9-mediated deletion of the PVL receptor, C5aR1, protected hiPSC-dMs from PVL cytotoxicity, despite the expression of other leukocidin receptors, such as CD45. PVL-deficient S. aureus had reduced ability to induce lung IL-1β levels in human C5aR1 knock-in mice. Unexpectedly, inhibiting NLRP3 activity resulted in increased wild-type S. aureus lung burdens. Our findings suggest that NLRP3 induces macrophage death and IL-1β secretion after PVL exposure and controls S. aureus lung burdens. (©2020 Society for Leukocyte Biology.) |
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| فهرسة مساهمة: | Keywords: NLRP3; inflammation; macrophage; pneumonia; staphylococcus; toxin |
| المشرفين على المادة: | 0 (Bacterial Proteins) 0 (Bacterial Toxins) 0 (C5AR1 protein, human) 0 (CD11b Antigen) 0 (Exotoxins) 0 (ITGAM protein, human) 0 (Interleukin-1beta) 0 (Leukocidins) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (NLRP3 protein, human) 0 (Panton-Valentine leukocidin) 0 (Peptide Fragments) 0 (Protein Subunits) 0 (Receptor, Anaphylatoxin C5a) 0 (Recombinant Proteins) 0 (leukocidin AB, Staphylococcus aureus) EC 3.1.3.48 (Leukocyte Common Antigens) EC 3.1.3.48 (PTPRC protein, human) |
| تواريخ الأحداث: | Date Created: 20200613 Date Completed: 20210209 Latest Revision: 20210209 |
| رمز التحديث: | 20231215 |
| DOI: | 10.1002/JLB.4MA0420-497R |
| PMID: | 32531864 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1938-3673 |
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| DOI: | 10.1002/JLB.4MA0420-497R |