Peptidoglycan and lipoteichoic acid from Staphylococcus aureus induce tumor necrosis factor alpha, interleukin 6 (IL-6), and IL-10 production in both T cells and monocytes in a human whole blood model
Peptidoglycan and lipoteichoic acid from Staphylococcus aureus induce tumor necrosis factor alpha, interleukin 6 (IL-6), and IL-10 production in both T cells and monocytes in a human whole blood model
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DOI：
10.1128/iai.68.7.3965-3970.2000
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发表时间：
2000-07-01
影响因子：
3.1
通讯作者：
Solberg, R
中科院分区：
文献类型：
--
作者：
Wang, JE;Jorgensen, PF;Solberg, R
我们检测了从金黄色葡萄球菌中分离的肽聚糖（PepG）和脂磷壁酸（LTA）诱导人全血中肿瘤坏死因子α（TNF-α）、白细胞介素-6（IL-6）和IL-10释放的能力，并鉴定了这些细胞因子的细胞来源。PepG和LTA均诱导血浆中TNF-α和IL-10的瞬时增加，分别在6和12 h达到峰值。IL-6值在整个实验期间（24 h）增加。由PepG和LTA诱导的TNF-α、IL-6和IL-10释放具有剂量依赖性。只有PepG是TNF-α分泌的有效诱导剂，用PepG或LTA刺激全血后，（CD 14阳性），T细胞（CD 2阳性），B细胞（CD 19阳性）和粒细胞（CD 15阳性）通过免疫磁性分离分离并通过逆转录-PCR分析编码TNF-α、IL-6和IL-10的mRNA转录物，TNF-α mRNA结果不确定。相反，PepG诱导T细胞和单核细胞中IL-6和IL-10 mRNA积累。LTA，以及脂多糖，诱导IL-6和IL-10的mRNA在单核细胞和可能在T细胞的生产。粒细胞和B细胞对细菌刺激是否产生细胞因子仍不清楚。用单克隆抗体（18 D11）阻断CD 14受体对PepG诱导的TNF-α的释放没有影响，但减弱了LTA诱导的相同细胞因子的释放。总之，我们的数据表明，循环T细胞和单核细胞有助于革兰氏阳性菌引起的脓毒症中细胞因子的产生。
We have examined the ability of peptidoglycan (PepG) and lipoteichoic acid (LTA) isolated from Staphylococcus aureus to induce the release of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and IL-10 in whole human blood and identified the cellular origins of these cytokines. Both PepG and LTA induced transient increases in TNF-alpha and IL-10 in plasma, with peak values at 6 and 12 h, respectively. IL-6 values increased throughout the experimental period (24 h), The TNF-alpha, IL-6, and IL-10 release induced by PepG and LTA was dose dependent. Only PepG was a potent inducer of TNF-or secretion, After stimulation of whole blood with PepG or LTA, very pure populations of monocytes (CD14 positive), T cells (CD2 positive), B cells (CD19 positive), and granulocytes (CD15 positive) were isolated by immunomagnetic separation and analyzed by reverse transcription-PCR for mRNA transcripts encoding TNF-alpha, IL-6, and IL-10, The TNF-alpha mRNA results were inconclusive, In contrast, PepG induced IL-6 and IL-10 mRNA accumulation in both T cells and monocytes. LTA, as well as lipopolysaccharide, induced IL-6 and IL-10 mRNA production in monocytes and possibly in T cells. Whether granulocytes and B cells produce cytokines in response to bacterial stimuli remains obscure. Blockade of the CD14 receptors with monoclonal antibodies (18D11) had no influence on the PepG induced release of TNF-alpha but attenuated the LTA-induced release of the same cytokine, In conclusion, our data indicate that circulating T cells and monocytes contribute to cytokine production in sepsis caused by grampositive bacteria.