Increased Reactive Oxygen Species Production by Peripheral Blood Mononuclear Leukocytes, not by Polymorphonuclear Leukocytes, in Atopic Dermatitis.
- Author:
Eun Ju HUH
1
;
Kyung Hwan RYU
;
Jae Kyun HUH
;
Jong Seo YOON
;
Young Hoon KIM
;
Jin Tack KIM
;
Hoon HAHN
;
Kweon Haeng LEE
;
Joon Sung LEE
Author Information
1. Department of Pediatrics, The Catholic University of Korea, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Atopic dermatitis;
Reactive oxygen species;
Mononuclear leukocytes;
Polymorphonuclear leukocyte
- MeSH:
Adenosine Triphosphate;
Dermatitis, Atopic*;
Humans;
Indicators and Reagents;
Inflammation;
Leukocytes, Mononuclear*;
Luminescence;
Neutrophils*;
Reactive Oxygen Species*;
Respiratory Burst
- From:Pediatric Allergy and Respiratory Disease
2004;14(1):53-61
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Reactive oxygen species (ROS) are known as a potential mediators that sustain chronic inflammation in atopic dermatitis (AD). To determine the role of peripheral blood mononuclear leukocytes (MO) and polymorphonuclear leukocytes (PMN) in prolonged inflammation, ROS generation of those cells in AD was examined. METHODS: Seventeen AD patients and 10 healthy controls were enrolled. MO and PMN were stimulated with the reagents: phobol ester (PMA), adenosine triphosphate (ATP), and chemotactic peptide (f-MLP). ROS levels were measured using chemiluminescence assay. RESULTS: In AD, chemiluminescence response of unstimulated MO was higher than that of normal controls. MO from AD patients produced 1.58-1.80 higher ROS for up to 30 minutes than the controls. When the cells were treated with the reagents (PMA, ATP, f-MLP), all the stimuli enhanced chemiluminescence activity of MO. When MO were treated with PMA, the ratio of ROS produced by MO of patients to that of the controls decreased. When the cells were treated with either ATP or f-MLP, the quantity of ROS generated by MO from the controls was greater than the controls. PMN from both AD patients and the controls generated ROS for 30 min similarly. As treated with the reagents, PMN from AD patients produced a smaller ROS than the controls. CONCLUSION: These results indicate MO but not PMN from AD patients were primed and ready for activation in vivo, and a reduced function of PMN from AD patients was observed. In conclusion, enhanced respiratory burst activity of MO is implicated in the prolonged inflammation of AD.
