ArticleScientific reports2020
Neutrophil elastase promotes macrophage cell adhesion and cytokine production through the integrin-Src kinases pathway.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- The immune-microbe-metal triad: a vicious cycle driving biomaterial corrosion in the oral inflammatory microenvironment.Bioactive materials · 2027Review
- Immature Neutrophil Phenotype and Enhanced Myeloperoxidase in Male Patients With Chronic Kidney Disease and Cardiovascular Comorbidity.Acta physiologica (Oxford, England) · 2026Article
- Neuro-immune-bone axis in post-traumatic bone regeneration: temporal regulation, dysregulation mechanisms, and therapeutic implications.Frontiers in immunology · 2026Review
- Global research trends in airway epithelial cell immune responses: a bibliometric study.Journal of thoracic disease · 2025Article
- Patients with persistent atrial fibrillation and metabolic comorbidities have an altered inflammatory state of atrial epicardial adipose tissue, which is linked to CT-attenuation.Cardiovascular diabetology · 2025Article
- Article
- Topography-based implants for bone regeneration: Design, biological mechanism, and therapeutics.Materials today. Bio · 2025Review
- Alpha-1 antitrypsin modulates neutrophil phenotype and function: implications for inflammatory regulation.Journal of leukocyte biology · 2025Article
- Dipeptidyl peptidase-1 inhibitors in bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Alterations of bone proteins in medication-related osteonecrosis of the jaw.European journal of oral sciences · 2025Article
- The heterogeneity of neutrophils in cancer and its implication for therapeutic targeting.Nature immunology · 2025Article
- Complement-mediated and direct activation of human neutrophils induced byFrontiers in immunology · 2025Article
- Neutrophil elastase activates macrophage calpain as a mechanism for phagocytic failure.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Immune cell regulatory networks in chronic obstructive pulmonary disease: mechanistic analysis from innate to adaptive immunity.Frontiers in immunology · 2025Review
- Targeting neutrophil serine proteases in bronchiectasis.The European respiratory journal · 2025Review
- Beyond the present: current and future perspectives on the role of infections in pediatric PCD.Frontiers in pediatrics · 2025Review
- Neutrophil Elastase Targets Select Proteins on Human Blood-Monocyte-Derived Macrophage Cell Surfaces.International journal of molecular sciences · 2024Article
- μMap-Interface: Temporal Photoproximity Labeling Identifies F11R as a Functional Member of the Transient Phagocytic Surfaceome.Journal of the American Chemical Society · 2024Article
- The role of neutrophils in chronic cough.Human cell · 2024Review
- Neutrophil serine proteases in cystic fibrosis: role in disease pathogenesis and rationale as a therapeutic target.European respiratory review : an official journal of the European Respiratory Society · 2024Review
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Authors and funding
5 authors.
Funding
Abstract
There are a number of respiratory diseases characterized by the presence of excess neutrophil elastase (NE) activity in tissues, including cystic fibrosis and chronic obstructive pulmonary disease (COPD). NE is considered a primary contributor to disease development, but the precise mechanism has yet to be fully determined. We hypothesized that NE alters the function of macrophages (Mɸ) which play a critical role in many physiological processes in healthy lungs. We demonstrate that monocyte-derived Mɸ exposed to NE releases active matrix metalloproteinases (MMPs), increase expression of pro-inflammatory cytokines TNFα, IL-1β, and IL-8, and reduce capacity to phagocytose bacteria. Changes in Mɸ function following NE treatment were accompanied by increased adhesion and cytoskeleton re-arrangement, indicating the possibility of integrin involvement. To support this observation, we demonstrate that NE induces phosphorylation of kinases from the Src kinase family, a hallmark of integrin signaling activation. Moreover, pretreatment of Mɸ with a specific Src kinase inhibitor, PP2 completely prevents NE-induced pro-inflammatory cytokine production. Taken together these findings indicate that NE participates in lung destruction not only through direct proteolytic degradation of matrix proteins, but also through activation of Mɸ inflammatory and proteolytic functions.
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Registered trials
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