Soltys J, Quinn M T
Department of Veterinary Molecular Biology, Montana State University, Bozeman 59717, USA.
Infect Immun. 1999 Jan;67(1):244-52. doi: 10.1128/IAI.67.1.244-252.1999.
Leukocytes activated by endotoxin or enterotoxins release proinflammatory cytokines, thereby contributing to the cascade of events leading to septic shock. In the present studies, we analyzed the effects of in vivo administration of a soluble immunomodulator, beta-(1,6)-branched beta-(1,3)-glucan (soluble beta-glucan), on toxin-stimulated cytokine production in monocytes and lymphocytes isolated from treated mice. In vitro stimulation of lymphocytes isolated from soluble beta-glucan-treated mice with lipopolysaccharide (LPS) resulted in enhanced production of interleukin-6 (IL-6) and suppressed production of tumor necrosis factor alpha (TNF-alpha), while stimulation of these cells with staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) resulted in enhanced production of gamma interferon (IFN-gamma) and suppressed production of IL-2 and TNF-alpha compared to that in cells isolated from untreated mice. In vitro stimulation of monocytes isolated from soluble beta-glucan-treated mice with LPS also resulted in suppressed TNF-alpha production, while stimulation of these cells with SEB or TSST-1 resulted in suppressed IL-6 and TNF-alpha production compared to that in cells isolated from untreated mice. Thus, the overall cytokine pattern of leukocytes from soluble beta-glucan-treated mice reflects suppressed production of proinflammatory cytokines, especially TNF-alpha. Taken together, our results suggest that treatment with soluble beta-glucan can modulate the induction cytokines during sepsis, resulting in an overall decrease in host mortality.
被内毒素或肠毒素激活的白细胞会释放促炎细胞因子，从而促使一系列导致感染性休克的事件发生。在本研究中，我们分析了体内给予可溶性免疫调节剂β-(1,6)-分支β-(1,3)-葡聚糖（可溶性β-葡聚糖）对从经治疗小鼠分离出的单核细胞和淋巴细胞中毒素刺激的细胞因子产生的影响。用脂多糖（LPS）体外刺激从经可溶性β-葡聚糖处理的小鼠分离出的淋巴细胞，导致白细胞介素-6（IL-6）产生增加，肿瘤坏死因子α（TNF-α）产生受到抑制，而用葡萄球菌肠毒素B（SEB）或中毒性休克综合征毒素1（TSST-1）刺激这些细胞，与从未经处理的小鼠分离出的细胞相比，γ干扰素（IFN-γ）产生增加，IL-2和TNF-α产生受到抑制。用LPS体外刺激从经可溶性β-葡聚糖处理的小鼠分离出的单核细胞，也导致TNF-α产生受到抑制，而用SEB或TSST-1刺激这些细胞，与从未经处理的小鼠分离出的细胞相比，IL-6和TNF-α产生受到抑制。因此，来自经可溶性β-葡聚糖处理的小鼠的白细胞的整体细胞因子模式反映出促炎细胞因子，尤其是TNF-α的产生受到抑制。综上所述，我们的结果表明，用可溶性β-葡聚糖治疗可调节脓毒症期间细胞因子的诱导，从而导致宿主死亡率总体下降。
