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KMID : 0370220070510010044
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Yakhak Hoeji
2007 Volume.51 No. 1 p.44 ~ p.50
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Differential Induction of Septic Shock by Lipopolyscchrides from E. coli and S. abortus
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Cho Jae-Youl
Yoo Eun-Sook
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Abstract
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Acute septic shock is one of inflammatory diseases mediated by pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α. In this study, we examined the pathological difference and mechanism of lipopolysaccharides isolated from E. coli (E-LPS) or S. abortus (S-LPS) on inducing acute septic shock in ICR mouse. All mice were died by intraperitoneal treatment of S-LPS with 0.75 mg/kg, whereas E-LPS treated with even 3 mg/kg only showed 30% of mice lethal, indicating that S-LPS may be more feasible in triggering a strong septic shock condition. The secretion pattern of TNF-α, a critical pro-inflammatory cytokine in septic shock condition, was also distinct between E-LPS-and S-LPS-treated groups. Thus, S-LPS strikingly increased serum level of TNF-α (6 ng/ml) at 1 h, while E-LPS just displayed at 2 ng/ml level. However, the interaction of S-LPS with LPS receptor, toll like receptor (TLR)-4 was not stronger than that of E-LPS, according to experiments with macrophage cell line RAW264.7 cells. Thus, E-LPS rather than S-LPS strongly enhanced the production of TNF-α. Interestingly, S-LPS more strongly up-regulated splenocyte proliferation, compared to E-LPS group, whereas there was no difference between S- or E-LPS treated groups in proliferation of Balb/c- or c57BL/6-originated splenic lymphocytes. Therefore, our data suggest that S-LPS is a more active endotoxin and that the strong septic shock-inducing effect of S-LPS seems due to the enhanccment of early TNF-α production and S-LPS sensitive lymphocyte proliferation.
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KEYWORD
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Septic Shock, LPS type, TNF-α, NO, splenic lymphocyte proliferation
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