Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Tumor necrosis factor causes bronchial hyperresponsiveness in rats.

J C Kips1, J Tavernier, R A Pauwels

  • 1Department of Respiratory Diseases, University Hospital, Ghent, Belgium.

The American Review of Respiratory Disease
|February 1, 1992
PubMed
Summary

Exposure to lipopolysaccharide (LPS) increases airway responsiveness by releasing tumor necrosis factor (TNF). TNF directly causes bronchial hyperresponsiveness and inflammation, as shown by increased neutrophils in bronchoalveolar lavage fluid.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Effect of Theophylline on Endotoxin and Tumor Necrosis Factor Induced Airway Changes in an in vivo Animal Model.

International archives of allergy and immunology·2021
Same author

Mutations in LZTR1 drive human disease by dysregulating RAS ubiquitination.

Science (New York, N.Y.)·2018
Same author

Compound A influences gene regulation of the Dexamethasone-activated glucocorticoid receptor by alternative cofactor recruitment.

Scientific reports·2017
Same author

Leptin receptor antagonism of iNKT cell function: a novel strategy to combat multiple myeloma.

Leukemia·2017
Same author

Getting RIDD of RNA: IRE1 in cell fate regulation.

Trends in biochemical sciences·2014
Same author

An overview of the safety of inhaled corticosteroids.

The International journal of risk & safety in medicine·2013

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Respiratory Physiology

Background:

  • Lipopolysaccharide (LPS) exposure in rats causes a transient increase in bronchial responsiveness (BR) to 5-hydroxytryptamine (5HT).
  • The role of tumor necrosis factor (TNF) in LPS-induced BR and airway inflammation remains unclear.

Purpose of the Study:

  • To investigate whether LPS induces TNF release in the airways.
  • To determine if TNF contributes to the LPS-induced increase in BR.
  • To assess TNF's effect on airway inflammation.

Main Methods:

  • Rats were exposed to aerosolized LPS or recombinant human TNF (rhTNF).
  • TNF concentrations in bronchoalveolar lavage (BAL) fluid were measured.
  • Bronchial responsiveness to 5HT was assessed.

Related Experiment Videos

  • Neutrophil influx into BAL fluid was quantified.
  • Anti-TNF antibodies were used for pretreatment.

    • Main Results:

    • LPS exposure led to dose-dependent increases in BAL TNF concentrations.
    • Exposure to rhTNF increased BR and induced neutrophil influx.
    • Anti-TNF antibodies significantly reduced LPS-induced BR and neutrophil influx.
    • TNF was not detected in saline-exposed control animals.

    Conclusions:

    • Tumor necrosis factor (TNF) is released in the airways following LPS exposure.
    • TNF directly contributes to bronchial hyperresponsiveness.
    • TNF plays a role in LPS-induced airway inflammation, characterized by neutrophil influx.