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R406 reduces lipopolysaccharide-induced neutrophil activation.
Warner, Seth; Teague, Heather L; Ramos-Benitez, Marcos J; Panicker, Sumith; Allen, Kiana; Gaihre, Salina; Moyer, Tom; Parachalil Gopalan, Bindu; Douagi, Iyadh; Shet, Arun; Kanthi, Yogendra; Suffredini, Anthony F; Chertow, Daniel S; Strich, Jeffrey R.
Afiliación
  • Warner S; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA.
  • Teague HL; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA.
  • Ramos-Benitez MJ; Basic Science Department, Microbiology Division, School of Medicine, Ponce Health Sciences University, Ponce, PR, USA.
  • Panicker S; Laboratory of Vascular Thrombosis and Inflammation, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
  • Allen K; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA.
  • Gaihre S; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA.
  • Moyer T; Flow Cytometry Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
  • Parachalil Gopalan B; Laboratory of Sickle Thrombosis and Vascular Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
  • Douagi I; Flow Cytometry Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA; NIH Center for Human Immunology, Inflammation, and Autoimmunity, National Institute of Allergy and Infectious Diseases, National Institutes o
  • Shet A; Laboratory of Sickle Thrombosis and Vascular Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
  • Kanthi Y; Laboratory of Vascular Thrombosis and Inflammation, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
  • Suffredini AF; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA.
  • Chertow DS; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA; Laboratory of Virology, National Institute o
  • Strich JR; Critical Care Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Critical Care Medicine Department, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD, USA. Electronic address: jeffrey.strich@nih.gov.
Cell Immunol ; 403-404: 104860, 2024.
Article en En | MEDLINE | ID: mdl-39084187
ABSTRACT
Modulating SYK has been demonstrated to have impacts on pathogenic neutrophil responses in COVID-19. During sepsis, neutrophils are vital in early bacterial clearance but also contribute to the dysregulated immune response and organ injury when hyperactivated. Here, we evaluated the impact of R406, the active metabolite of fostamatinib, on neutrophils stimulated by LPS. We demonstrate that R406 was able to effectively inhibit NETosis, degranulation, ROS generation, neutrophil adhesion, and the formation of CD16low neutrophils that have been linked to detrimental outcomes in severe sepsis. Further, the neutrophils remain metabolically active, capable of releasing cytokines, perform phagocytosis, and migrate in response to IL-8. Taken together, this data provides evidence of the potential efficacy of utilizing fostamatinib in bacterial sepsis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Lipopolisacáridos / Activación Neutrófila / Aminopiridinas / Neutrófilos Límite: Humans Idioma: En Revista: Cell Immunol Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Lipopolisacáridos / Activación Neutrófila / Aminopiridinas / Neutrófilos Límite: Humans Idioma: En Revista: Cell Immunol Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos