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

Acute joint inflammation--mechanisms and mediators

D T Scott1, F Y Lam, W R Ferrell

  • 1Institute of Physiology, University of Glasgow, Scotland.

General Pharmacology
|November 1, 1994
PubMed
Summary

Sensory neuropeptides like substance P (SP) and calcitonin gene-related peptide (CGRP) significantly contribute to acute joint inflammation by increasing vascular permeability and blood flow. The sympathetic nervous system shows minimal involvement in acute inflammatory joint conditions.

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

PAR2 deletion in the osteoblast lineage affords long-term cartilage protection in experimental osteoarthritis.

Osteoarthritis and cartilage·2026
Same author

Moderate exercise protects against joint disease in a murine model of osteoarthritis.

Frontiers in physiology·2022
Same author

PAR(2) expression in peripheral blood monocytes of patients with rheumatoid arthritis.

Annals of the rheumatic diseases·2012
Same author

Proteinase-activated receptor-2 mediated inhibition of TNFalpha-stimulated JNK activation - A novel paradigm for G(q/11) linked GPCRs.

Cellular signalling·2009
Same author

Angiotensin receptor blockers reduce erythrocyte sedimentation rate levels in patients with rheumatoid arthritis.

Annals of the rheumatic diseases·2008
Same author

Strain dependence in murine models of monoarthritis.

Inflammation research : official journal of the European Histamine Research Society ... [et al.]·2008

Area of Science:

  • Rheumatology
  • Neuroimmunology
  • Inflammation Research

Background:

  • Acute joint inflammation involves numerous mediators, including cytokines, eicosanoids, complement, kinin systems, histamine, and serotonin.
  • Sensory neuropeptides, specifically substance P (SP) and calcitonin gene-related peptide (CGRP), are recognized as important contributors to inflammatory processes.

Purpose of the Study:

  • To review the role of various mediators in acute joint inflammation.
  • To specifically highlight the contribution of sensory neuropeptides to the pathogenesis of acute arthritis.

Main Methods:

  • Literature review of factors contributing to acute joint inflammation.
  • Analysis of the role of neuropeptides in joint innervation and inflammatory responses.

Related Experiment Videos

Main Results:

  • Pro-inflammatory neurokinins, SP and CGRP, found in joint-innervating nerves, significantly increase vascular permeability and hyperemia in acute arthritis.
  • Cytokines, eicosanoids, complement, kinin systems, histamine, and 5-hydroxytryptamine are also key mediators of inflammation.
  • The sympathetic nervous system appears to have limited involvement in acute inflammatory joint disease models.

Conclusions:

  • Sensory neuropeptides SP and CGRP play a crucial role in the vascular changes associated with acute joint inflammation.
  • While involved in chronic conditions, the sympathetic nervous system's role in acute joint inflammation is minimal.