Neutrophil Apoptosis and H2O2 Release by LPS in Diabetics / 결핵및호흡기질환
Tuberculosis and Respiratory Diseases
; : 250-256, 2004.
Article
em Ko
| WPRIM
| ID: wpr-152130
Biblioteca responsável:
WPRO
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.
Palavras-chave
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Infecções Bacterianas
/
Sobrevivência Celular
/
Mortalidade
/
Explosão Respiratória
/
Apoptose
/
Flebotomia
/
Voluntários Saudáveis
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Peróxido de Hidrogênio
/
Inflamação
/
Neutrófilos
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
Ko
Revista:
Tuberculosis and Respiratory Diseases
Ano de publicação:
2004
Tipo de documento:
Article