ArticleThe Journal of clinical investigation1989
Complement receptor expression on neutrophils at an inflammatory site, the Pseudomonas-infected lung in cystic fibrosis.
Article in The Journal of clinical investigation, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 209 citations in OpenAlex.
- Altered Degranulation and pH of Neutrophil Phagosomes Impacts Antimicrobial Efficiency in Cystic Fibrosis.Frontiers in immunology · 2020Trial
- Anti-PcrV antibody in cystic fibrosis: a novel approach targeting Pseudomonas aeruginosa airway infection.Pediatric pulmonology · 2014Trial
- Galectin-9 signaling through TIM-3 is involved in neutrophil-mediated Gram-negative bacterial killing: an effect abrogated within the cystic fibrosis lung.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Trial
- Hyperconcentrated mucus in small airways: a mechanistic model for the pathogenesis of paediatric bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Pseudomonas infections persisting after CFTR modulators are widespread throughout the lungs and drive lung inflammation.Cell host & microbe · 2025Article
- Neutrophil elastase activates macrophage calpain as a mechanism for phagocytic failure.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Review
- Subversion of the Complement System by Pseudomonas aeruginosa.Journal of bacteriology · 2023Review
- Competitive survival of clonal serialiScience · 2023Article
- Diagnosis and Management of Cystic Fibrosis Exacerbations.Seminars in respiratory and critical care medicine · 2023Review
- Roles of neutrophil granule proteins in orchestrating inflammation and immunity.The FEBS journal · 2022Review
- Mucus Clearance Strategies in Mechanically Ventilated Patients.Frontiers in physiology · 2022Review
- Targeting Neutrophils for Promoting the Resolution of Inflammation.Frontiers in immunology · 2022Review
- C3d Elicits Neutrophil Degranulation and Decreases Endothelial Cell Migration, with Implications for Patients with Alpha-1 Antitrypsin Deficiency.Biomedicines · 2021Article
- Neutrophil heterogeneity and fate in inflamed tissues: implications for the resolution of inflammation.American journal of physiology. Cell physiology · 2020Article
- 15-Epi-LXAProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Viral Evasion of the Complement System and Its Importance for Vaccines and Therapeutics.Frontiers in immunology · 2020Review
- A versatile high-throughput assay to characterize antibody-mediated neutrophil phagocytosis.Journal of immunological methods · 2019Article
- The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals.Journal of inflammation research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Activation of human neutrophils (PMN) is accompanied by rapid upregulation of CR1, the C3b receptor, and CR3, the iC3b receptor, which also serves as the PMN's major adherence protein. This is necessary for migration and phagocytosis, but the extent of expression of these proteins on PMN at inflammatory sites has not been determined. We used monoclonal antibodies and flow cytometry to assess CR1 and CR3 expression on PMN in bronchoalveolar lavage (BAL) fluid of cystic fibrosis (CF) patients chronically infected with pseudomonas and in sterile joint fluid of arthritis patients. Resting peripheral blood PMN from these patients and normals expressed similar low levels of CR1 and CR3, and the patients' PMN increased CR1 and CR3 expression normally when stimulated in vitro. CR3 expression on CF BAL PMN was 90 +/- 12% of that on the same patient's blood cells stimulated in vitro with FMLP. In contrast, CR1 expression on BAL PMN was only 27 +/- 8% of that on stimulated blood cells. Similar results were obtained for joint PMN. This pattern could be reproduced in vitro by treating FMLP-stimulated blood cells with BAL supernatants or with pseudomonas or PMN elastase. The serine protease inhibitors, PMSF and alpha 1-antitrypsin prevented the lavage supernatant from reducing CR1 expression, while metalloprotease inhibitors had no effect. Treatment of PMN with elastase in vitro decrease their ability to kill opsonized Pseudomonas aeruginosa. These results suggest that PMN at inflammatory sites have maximally upregulated expression of their complement receptors, but that CR1 is then cleaved by proteolysis in situ. Although not related to the basic defect in CF, this may interfere with efficient phagocytosis and contribute to the CF patient's inability to eradicate chronic lung infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.