ArticleScientific reports2019
G-CSFR antagonism reduces neutrophilic inflammation during pneumococcal and influenza respiratory infections without compromising clearance.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Spectral Flow Cytometry Method for Immunophenotyping Neutrophil Activation and NETs in an Acute Dust Exposure Model.Immunity, inflammation and disease · 2026Article
- Immature neutrophils are elevated in human PGD and linked to G-CSF-driven injury in a murine model of lung ischemia-reperfusion.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026Article
- G-CSF/NAMPT signaling drives neutrophil dysfunction and enhances bacterial infection susceptibility in cancer patients.Nature communications · 2025Article
- Csk-mediated Src family kinase regulation dampens neutrophil infiltration during pulmonary infection.JCI insight · 2025Article
- Targeted labeling and depletion of alveolar macrophages using VeDTR mouse technology.iScience · 2025Article
- Hyaluronic acid synthase 2 dysfunction exacerbates elastase-induced neutrophilic airway inflammation and emphysema in mice.Frontiers in immunology · 2025Article
- Neutrophil reduction attenuates the severity of lung injury in the early phase of pneumococcal pneumonia in mice.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Clinical features and risk factors of primary Sjögren's syndrome complicated with severe pneumonia: a case-control study.Clinical rheumatology · 2024Article
- The granulocyte colony-stimulating factor produced duringFrontiers in immunology · 2024Article
- Neutrophil Extracellular Traps in Breast Cancer: Roles in Metastasis and Beyond.Journal of Cancer · 2024Review
- Preclinical Study in Mouse Thymus and Thymocytes: Effects of Treatment with a Combination of Sodium Dichloroacetate and Sodium Valproate on Infectious Inflammation Pathways.Pharmaceutics · 2023Article
- The Therapeutic Treatment with the GAG-Binding Chemokine Fragment CXCL9(74-103) Attenuates Neutrophilic Inflammation and Lung Dysfunction duringInternational journal of molecular sciences · 2022Article
- Interleukin-6 and granulocyte colony-stimulating factor as predictors of the prognosis of influenza-associated pneumonia.BMC infectious diseases · 2022Article
- Influenza A Virus-Driven Airway Inflammation may be Dissociated From Limb Muscle Atrophy in Cigarette Smoke-Exposed Mice.Frontiers in pharmacology · 2022Article
- Neutrophils at the crossroads of acute viral infections and severity.Molecular aspects of medicine · 2021Review
- Review
- A Fragile Balance: Does Neutrophil Extracellular Trap Formation Drive Pulmonary Disease Progression?Cells · 2021Review
- Neutrophils in Tumorigenesis: Missing Targets for Successful Next Generation Cancer Therapies?International journal of molecular sciences · 2021Review
- Leukocyte trafficking to the lungs and beyond: lessons from influenza for COVID-19.Nature reviews. Immunology · 2021Review
- G-CSF and GM-CSF Are Different. Which One Is Better for COVID-19?Acta haematologica · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive neutrophilic inflammation can contribute to the pathogenesis of pneumonia. Whilst anti-inflammatory therapies such as corticosteroids are used to treat excessive inflammation, they do not selectively target neutrophils and may compromise antimicrobial or antiviral defences. In this study, neutrophil trafficking was targeted with a granulocyte-colony stimulating factor receptor monoclonal antibody (G-CSFR mAb) during Streptococcus pneumoniae (serotype 19F) or influenza A virus (IAV, strain HKx31) lung infection in mice. Firstly, we demonstrated that neutrophils are indispensable for the clearance of S. pneumoniae from the airways using an anti-Ly6G monoclonal antibody (1A8 mAb), as the complete inhibition of neutrophil recruitment markedly compromised bacterial clearance. Secondly, we demonstrated that G-CSF transcript lung levels were significantly increased during pneumococcal infection. Prophylactic or therapeutic administration of G-CSFR mAb significantly reduced blood and airway neutrophil numbers by 30-60% without affecting bacterial clearance. Total protein levels in the bronchoalveolar lavage (BAL) fluid (marker for oedema) was also significantly reduced. G-CSF transcript levels were also increased during IAV lung infection. G-CSFR mAb treatment significantly reduced neutrophil trafficking into BAL compartment by 60% and reduced blood neutrophil numbers to control levels in IAV-infected mice. Peak lung viral levels at day 3 were not altered by G-CSFR therapy, however there was a significant reduction in the detection of IAV in the lungs at the day 7 post-infection phase. In summary, G-CSFR signalling contributes to neutrophil trafficking in response to two common respiratory pathogens. Blocking G-CSFR reduced neutrophil trafficking and oedema without compromising clearance of two pathogens that can cause pneumonia.
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