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Altered Ca2+ signalling in human neutrophils from inflammatory sites
E V Davies1, B D Williams, R J Whiston
1Department of Surgery, University of Wales, College of Medicine, Cardiff, United Kingdom.
Annals of the Rheumatic Diseases
|July 1, 1994
Summary
Neutrophils from patients with rheumatoid arthritis, joint disease, and leg ulcers show increased intracellular calcium (Ca2+) release at inflammatory sites. This heightened Ca2+ release may contribute to increased neutrophil oxidase activation in these conditions.
Area of Science:
- Immunology
- Cell Biology
- Rheumatology
Background:
- Neutrophils play a critical role in inflammatory responses.
- Aberrant calcium signaling in neutrophils is implicated in various inflammatory diseases.
Purpose of the Study:
- To investigate differences in intracellular calcium (Ca2+) store release in neutrophils from patients with rheumatoid arthritis, other joint diseases, and leg ulcers compared to healthy individuals.
Main Methods:
- Ratiometric imaging of fura2 was employed to quantify Ca2+ release into the cytosol of individual neutrophils.
- Measurements were taken from neutrophils in circulation and synovial fluid.
Main Results:
- Neutrophils from synovial fluid of rheumatoid arthritis and other joint disease patients, as well as those from leg ulcers, exhibited significantly increased cytosolic Ca2+.
- Circulating neutrophils from rheumatoid arthritis patients showed a trend towards increased Ca2+ release (p=0.09).
Conclusions:
- Elevated cytosolic Ca2+ release at inflammatory sites in neutrophils is observed in rheumatoid arthritis, other joint diseases, and leg ulcers.
- This increased Ca2+ release is hypothesized to enhance neutrophil oxidase activation, contributing to disease pathogenesis.