Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Aging (Upcoming)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI114699

Neutrophil elastase cleaves C3bi on opsonized pseudomonas as well as CR1 on neutrophils to create a functionally important opsonin receptor mismatch.

M F Tosi, H Zakem, and M Berger

Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.

Find articles by Tosi, M. in: JCI | PubMed | Google Scholar

Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.

Find articles by Zakem, H. in: JCI | PubMed | Google Scholar

Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.

Find articles by Berger, M. in: JCI | PubMed | Google Scholar

Published July 1, 1990 - More info

Published in Volume 86, Issue 1 on July 1, 1990
J Clin Invest. 1990;86(1):300–308. https://doi.org/10.1172/JCI114699.
© 1990 The American Society for Clinical Investigation
Published July 1, 1990 - Version history
View PDF
Abstract

Neutrophil elastase has been implicated as a factor that impairs local host defenses in chronic Pseudomonas aeruginosa (Pa) lung infection in cystic fibrosis (CF). We recently showed that this enzyme cleaves the C3b receptor, CR1, from neutrophils (PMN) in the lungs of infected CF patients. The C3bi receptor on these cells, CR3, is resistant to elastase. We now show that purified neutrophil elastase markedly impairs complement-mediated PMN-Pa interactions including phagocytosis of opsonized Pa, stimulation by opsonized Pa of PMN superoxide production, and killing of opsonized Pa by PMN. When PMN and opsonized Pa were treated separately with elastase, additive levels of inhibition were observed in each of the above assays. The effects on the bacteria were due to cleavage of the bound C3bi from the surface of opsonized Pa by neutrophil elastase. C3bi was also cleaved by pseudomonas elastase, or bronchoalveolar lavage fluid from CF patients with chronic Pa lung infection. Inhibitors of neutrophil elastase eliminated C3bi cleavage by BAL fluid, while inhibitors of pseudomonas elastase had no effect. Blocking CR1 and CR3 on PMN with specific monoclonal antibodies reduced phagocytosis of opsonized Pa to an extent similar to that caused by elastase cleavage of CR1 on PMN and C3bi on Pa. We conclude that neutrophil elastase in the lungs of chronically infected CF patients cleaves C3bi from opsonized Pa as well as CR1 from PMN, creating an "opsonin-receptor mismatch" that severely impairs complement-mediated phagocytic host defenses against these bacteria.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 300
page 300
icon of scanned page 301
page 301
icon of scanned page 302
page 302
icon of scanned page 303
page 303
icon of scanned page 304
page 304
icon of scanned page 305
page 305
icon of scanned page 306
page 306
icon of scanned page 307
page 307
icon of scanned page 308
page 308
Version history
  • Version 1 (July 1, 1990): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts