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| http://dx.doi.org/10.1183/13993003.01512-2023 | DOI Listing |
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Neutrophil elastase-dependent cleavage of LTA4H alters its aminopeptidase activity in cystic fibrosis.
Eur Respir J
March 2024
Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
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View Article and Find Full Text PDFDiminished airway host innate response in people with cystic fibrosis who experience frequent pulmonary exacerbations.
Eur Respir J
February 2024
Belfast Health and Social Care Trust, Belfast, UK
Rationale: Pulmonary exacerbations are clinically impactful events that accelerate cystic fibrosis (CF) lung disease progression. The pathophysiological mechanisms underlying an increased frequency of pulmonary exacerbations have not been explored.
Objectives: To compare host immune response during intravenous antibiotic treatment of pulmonary exacerbations in people with CF who have a history of frequent infrequent exacerbations.
An in vivo model for extracellular vesicle-induced emphysema.
JCI Insight
January 2022
Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine.
Chronic obstructive pulmonary disease (COPD) is a debilitating chronic disease and the third-leading cause of mortality worldwide. It is characterized by airway neutrophilia, promoting tissue injury through release of toxic mediators and proteases. Recently, it has been shown that neutrophil-derived extracellular vesicles (EVs) from lungs of patients with COPD can cause a neutrophil elastase-dependent (NE-dependent) COPD-like disease upon transfer to mouse airways.
View Article and Find Full Text PDFInhibition of Efferocytosis by Extracellular CIRP-Induced Neutrophil Extracellular Traps.
J Immunol
February 2021
Center for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY 11030;
Phagocytic clearance of apoptotic cells by the macrophages (efferocytosis) is impaired in sepsis, but its mechanism is poorly understood. Extracellular cold-inducible RNA-binding protein (eCIRP) is a novel damage-associated molecular pattern that fuels inflammation. We identify that eCIRP-induced neutrophil extracellular traps (NETs) impair efferocytosis through a novel mechanism.
View Article and Find Full Text PDFHeparin induces neutrophil elastase-dependent vital and lytic NET formation.
Int Immunol
May 2020
Laboratory of Malaria Immunology, Yamada-oka, Suita, Osaka, Japan.
Heparin is used extensively as an anticoagulant in a broad range of diseases and procedures; however, its biological effects are not limited to coagulation and remain incompletely understood. Heparin usage can lead to the life-threatening complication known as heparin-induced thrombocytopenia (HIT), caused by the development of antibodies against heparin/PF4 complexes. Here, we demonstrate the ability of heparin to induce neutrophil extracellular traps (NETs).
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