Related Experiment Videos
Superoxide production by peripheral polymorphonuclear leukocytes in patients with COPD
W J C van Beurden1, P L M L Wielders, P J T Scheepers
1Department of Pulmonary Diseases, Catharina Hospital, Eindhoven, The Netherlands. wendy@beurdenvan.myweb.nl
Respiratory Medicine
|April 16, 2003
Summary
Polymorphonuclear leukocytes (PMNs) in COPD patients show increased superoxide anion release when exposed to ultrafine carbon black particles. This suggests PMNs in COPD may be more susceptible to stimulation by fine particulate matter.
Area of Science:
- Pulmonary Medicine
- Immunology
- Environmental Health
Background:
- Polymorphonuclear leukocytes (PMNs) contribute to Chronic Obstructive Pulmonary Disease (COPD) pathogenesis through oxidant release, such as superoxide anion (SA).
- Understanding PMN responses to environmental stimuli is crucial for COPD management.
Purpose of the Study:
- To quantify spontaneous and stimulated SA release from peripheral PMNs in stable COPD patients compared to healthy controls.
- To investigate the effect of various particulate matter stimuli on PMN SA release.
Main Methods:
- Peripheral PMNs were isolated from 17 stable COPD patients and 17 age-matched healthy controls.
- SA release was measured spectrophotometrically using the superoxide dismutase (SOD) inhibitable reduction of cytochrome c.
- PMNs were stimulated with phorbol myristate acetate (PMA), diesel exhaust particles (DEPs), carbon black (CB), and ultrafine CB (ufCB).
Main Results:
- Spontaneous SA release was comparable between COPD patients and controls.
- PMA stimulation increased SA release in both groups.
- DEPs and CB did not significantly alter SA release in either group.
- Ultrafine CB significantly increased SA release only in the COPD patient group.
Conclusions:
- COPD patient PMNs exhibit heightened SA release upon stimulation with ultrafine carbon black particles.
- The smaller particle size of ufCB appears to be a critical factor in this enhanced PMN response.
- These findings suggest increased PMN susceptibility to certain environmental stimuli in COPD.