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Heat-killed Staphylococcus aureus induces a common early response in human monocytes in the presence of high concentration glucose / 中华微生物学和免疫学杂志
Chinese Journal of Microbiology and Immunology ; (12): 1005-1010, 2012.
Artículo en Chino | WPRIM | ID: wpr-429352
ABSTRACT
Objective To investigate the effects of heat-killed Staphylococcus aureus (HKSA) on the apoptosis and expression of iNOS and IL-1β in THP-1 monocytes in the presence of high concentration of glucose.Methods THP-1 cells were cultured in medium containing 25.0 mmol/L(HG) or 5.5 mmol/L (LG,control) D-glucose for 12 h-8 d.The THP-1 cells cultured for 6 d were extracted on the 0-48 h with or without HKSA,then apoptosis and expression of iNOS and IL-1β were examined.Apoptosis was analyzed by flow cytometry and expressions of IL-1β and iNOS were quantitated by real-time PCR.Results The expression of iNOS and IL-1β in THP-1 monocytes was increased significantly in the presence of high concentration of glucose for 12-48 h(P<0.05),reaching the highest level at 24 h and returned to baseline after 4 d.The expression was significantly lower than that of control after 4-6 d.Apoptosis rate was also increased significantly after 48 h to 4 days.HKSA infection enhanced apoptosis,but inhibited the expression of iNOS and IL-1 β in the presence of high concentration of glucose.The expression of iNOS and IL-1β increased significantly at 6 h(P<0.01),reaching the highest level at 12 h,but the levels were significantly lower than those in control groups (P<0.05).Conclusion These data suggest that high concentration of glucose can interfere with the anti-bacterial function of monocytes by reducing their expression of iNOS and IL-1β and enhancing their apoptosis.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Microbiology and Immunology Año: 2012 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Microbiology and Immunology Año: 2012 Tipo del documento: Artículo