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

Effect of beta-receptor stimulation on Kupffer cell complement receptor clearance function.

D J Loegering1, L M Commins

  • 1Department of Physiology, Albany Medical College, NY 12208.

Circulatory Shock
|August 1, 1988
PubMed
Summary
This summary is machine-generated.

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

Peptide-based analysis of amino acid sequences important to the biological activity of eosinophil granule major basic protein.

Immunology letters·2001
Same author

Fcgamma-receptor signaling augments the LPS-stimulated increase in serum tumor necrosis factor-alpha levels.

American journal of physiology. Regulatory, integrative and comparative physiology·2001
Same author

Differential requirement for classic and novel PKC isoforms in respiratory burst and phagocytosis in RAW 264.7 cells.

Journal of immunology (Baltimore, Md. : 1950)·2000
Same author

IgG-coated erythrocytes augment LPS-stimulated TNF-alpha secretion, TNF-alpha mRNA levels, and TNF-alpha mRNA stability in macrophages.

Biochemical and biophysical research communications·2000
Same author

Role of an oxidative stress in the macrophage dysfunction caused by erythrophagocytosis.

Free radical biology & medicine·2000
Same author

A phagocytic challenge with IgG-coated erythrocytes depresses macrophage respiratory burst and phagocytic function by different mechanisms.

Journal of leukocyte biology·1999

Increased sympathetic activity, triggered by injury, depresses Kupffer cell complement receptor function. Beta-receptor stimulation by catecholamines contributes to this impairment, affecting immune responses.

Area of Science:

  • Immunology
  • Physiology
  • Pharmacology

Background:

  • Kupffer cell complement receptor function is crucial for immune responses.
  • Experimental injuries often lead to depressed Kupffer cell function.
  • In vitro studies suggest beta-receptor stimulation impairs macrophage function.

Purpose of the Study:

  • To investigate if increased sympathetic activity post-injury contributes to depressed Kupffer cell complement receptor function.
  • To determine the role of beta-adrenergic stimulation in Kupffer cell dysfunction.

Main Methods:

  • Assessed Kupffer cell complement receptor function in rats via hepatic uptake of IgM-coated erythrocytes.
  • Administered varying doses of isoproterenol, norepinephrine, and epinephrine.
  • Utilized beta-receptor blockade with propranolol to assess its protective effects.

Related Experiment Videos

  • Induced thermal injury to evaluate its impact on receptor function.

    • Main Results:

    • Isoproterenol infusion depressed Kupffer cell receptor function at 5.0 and 0.5 µg/kg/min, but not 0.05 µg/kg/min.
    • Isoproterenol, norepinephrine, and epinephrine (0.5 µg/kg/min) reduced receptor function by 41%, 38%, and 29%, respectively.
    • Beta-receptor blockade prevented isoproterenol- and norepinephrine-induced depression.
    • Thermal injury caused a 65% depression in receptor function, reduced to 35% with beta-receptor blockade.

    Conclusions:

    • Increased circulating catecholamines, via beta-receptor stimulation, likely contribute to Kupffer cell dysfunction after injury.
    • Targeting beta-adrenergic pathways may offer a therapeutic strategy to mitigate immune suppression post-injury.