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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Interleukin 8 Secretion from Monocytes of Subjects Heterozygous for the ΔF508 Cystic Fibrosis Transmembrane Conductance Regulator Gene Mutation Is Altered
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Interleukin 8 Secretion from Monocytes of Subjects Heterozygous for the ΔF508 Cystic Fibrosis Transmembrane Conductance Regulator Gene Mutation Is Altered

机译：ΔF508囊性纤维化跨膜电导调节基因突变的受试者杂合子单核细胞的白细胞介素8分泌被改变。

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Patients with cystic fibrosis (CF) exhibit an excessive host inflammatory response. The aim of this study was to determine (i) whether interleukin 8 (IL-8) secretion is increased from monocytes from subjects heterozygous as well as homozygous for cystic fibrosis transmembrane conductance regulator (CFTR) mutations and (ii) whether this is due to increased cell surface lipopolysaccharide (LPS) receptors or, alternatively, increased activation of mitogen-activated protein kinases (MAPK). The basal level of IL-8 secretion was higher from monocytes from CF patients than from monocytes from healthy controls (P = 0.02) and obligate heterozygotes (parents of the CF patients). The 50% effective concentrations for LPS-induced IL-8 production for monocytes from both CF patients and obligate heterozygotes were 100-fold lower than those for monocytes from healthy controls (P < 0.05). No differences in the levels of IL-1β production were seen between these groups. Expression of the LPS surface receptors CD14 and Toll-like receptor 4 were not different between CF patients and healthy controls. In contrast, phosphorylation of the MAPKs p38 and ERK occurred at lower doses of LPS in monocytes from patients heterozygous and homozygous for CFTR mutations. These results indicate that a single allelic CFTR mutation is sufficient to augment IL-8 secretion in response to LPS. This is not a result of increased LPS receptor expression but, rather, is associated with alterations in MAPK signaling.
机译：囊性纤维化（CF）患者表现出过度的宿主炎症反应。这项研究的目的是确定（i）囊性纤维化跨膜电导调节剂（CFTR）突变的杂合子和纯合子的单核细胞中白细胞介素8（IL-8）的分泌是否增加，以及（ii）这是否是由于增加细胞表面脂多糖（LPS）受体，或者增加促分裂原活化蛋白激酶（MAPK）的活化。 CF患者单核细胞的IL-8分泌基础水平高于健康对照组（ P = 0.02）和专性杂合子（CF患者的父母）的单核细胞。 CF患者和专性杂合子对LPS诱导的IL-8产生的50％有效浓度比健康对照对单核细胞的有效浓度低100倍（ P <0.05）。这些组之间没有观察到IL-1β产生水平的差异。在CF患者和健康对照之间，LPS表面受体CD14和Toll样受体4的表达没有差异。相反，来自CFTR突变的杂合和纯合患者的单核细胞中LPS剂量较低时，MAPKs p38和ERK发生磷酸化。这些结果表明，单个等位基因CFTR突变足以增强对LPS的IL-8分泌。这不是LPS受体表达增加的结果，而是与MAPK信号传导的改变有关。

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