Exposure to Toluene Diisocyanate (TDI) Induces IL-8 Production from Bronchial Epithelial Cells: Effect of Pro-inflammatory Cytokines
Journal of Korean Medical Science
;
: 809-812, 2003.
Artículo
en Inglés
| WPRIM
| ID: wpr-187040
ABSTRACT
This investigation was designed to confirm IL-8 production from human bronchial epithelial cells with toluene diisocyanate (TDI) exposure and to examine the effects of pro-inflammatory cytokine and dexamethasone. We cultured Beas-2B, a bronchial epithelial cell line with TDI-HSA conjugate and compared with those without conjugate. IL-8 in the supernatant was measured by ELISA. To evaluate the effect of proinflammatory cytokines, peripheral blood mononuclear cells (PBMC) were collected from TDI- and non-TDI asthma patients, and were added to the epithelial cell culture. Dexamethasone or antibodies to TNF-alpha and IL-1beta were pre-incubated with PBMC supernatant. There was a significant production of IL-8 from bronchial epithelial cells with addition of TDI-HSA conjugate in a dose-dependent manner, which was significantly augmented with addition of PBMC supernatant. Higher production of IL-8 was noted with addition of PBMC supernatant from TDI-asthma patients than in those from non-TDI asthma patients. IL-1beta and IL-1beta/TFNalpha antibodies were able to suppress the IL-8 productions. Pre-treatment of dexamethasone induced dose-dependent inhibition of the IL-8 production. These results suggest that the IL-8 production from bronchial epithelial cells contribute to neutrophil recruitment occurring in TDIinduced airway inflammation. IL-1beta released from PBMC of TDI-induced asthma patients may be one of the pro-inflammatory cytokines to enhance IL-8 production.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Asma
/
Bronquios
/
Dexametasona
/
Leucocitos Mononucleares
/
Línea Celular
/
Interleucina-8
/
2,4-Diisocianato de Tolueno
/
Células Epiteliales
/
Glucocorticoides
Límite:
Humanos
Idioma:
Inglés
Revista:
Journal of Korean Medical Science
Año:
2003
Tipo del documento:
Artículo
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