내독소로 자극된 당뇨환자의 중성구에서 기획성 세포사멸과 과산화수소 분비능
- Alternative Title
- Neutrophil Apoptosis and H2O2 Release by LPS in Diabetics
- Abstract
- Background : Bacterial infections in diabetic patients are an important cause of increased morbidity and mortality. It has been reported that bacterial infections in diabetics showed more impaired PMN functions such as reduced PMN respiratory burst and decreased microbicidal activity in inflammed tissues. Also, apoptosis(programmed cell death) is postulated to be a key mechanism for neutrophil elimination. It is very important that PMN apoptosis keeps the balance from an area of inflammation. Actuallly, as little was known about PMN apoptosis and respiratory burst in diabetes, we investigated PMN apoptosis and hydrogen peroxide production after endotoxin exposure. Methods : Peripheral venous blood samples were collected by routine venipuncture from healthy volunteers and diabetics to harvest neutrophils. We respectively measured the PMN apoptosis, the production of hydrogen peroxide, and the cell viability. Results : Normal neutrophils showed a tendency to decreased apoptosis after endotoxin treatment. In patients with diabetes, PMN apoptosis was significantly decreased compared with healthy controls. In addition, the LPS-induced neutrophils in diabetics demonstrated more decreased apoptosis. However, the production of hydrogen peroxide was not different between groups. Conclusion : These observations suggest that the decreased PMN apoptosis in diabetics with endotoxin exposure may also affect the increased susceptibility and severity of infections.
- All Author(s)
- 서기현
; 나주옥
; 문승혁
; 어수택
; 김용훈
; 박춘식
- Issued Date
- 2004
- Type
- Article
- Keyword
- LPS(lipopolysaccharide); PMN apoptosis; hydrogen peroxide; Diabetes
- Publisher
- 대한결핵및호흡기학회
- ISSN
- 0378-0066
; 1738-3536
; 2005-6184
- Citation Title
- 결핵 및 호흡기질환
Tuberculosis and Respiratory Disease
- Citation Volume
- 57
- Citation Number
- 3
- Citation Start Page
- 250
- Citation End Page
- 256
- Language(ISO)
- kor
- DOI
- 10.4046/trd.2004.57.3.250
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/668
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