Increased secretion of pro-inflammatory cytokines by circulating polymorphonuclear neutrophils and regulation by interleukin 10 during intestinal inflammation
Increased secretion of pro-inflammatory cytokines by circulating polymorphonuclear neutrophils and regulation by interleukin 10 during intestinal inflammation
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DOI：
10.1136/gut.42.4.470
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发表时间：
1998-04-01
期刊：
影响因子：
24.5
通讯作者：
Schreiber, S
中科院分区：
文献类型：
--
作者：
Nikolaus, S;Bauditz, J;Schreiber, S
背景：活动性炎症性肠病（FED）患者的肠粘膜中促炎细胞因子的浓度增加。中性粒细胞（PMN）是IBD肠道病变中最丰富的细胞类型。白细胞介素10（IL-10）是一种重要的抗炎细胞因子，可诱导促炎细胞因子的下调，目的：研究UBD和感染性结肠炎患者的中性粒细胞（PMN）是否分泌大量促炎细胞因子，并通过IL-10进行调节。在外周PMN中评估促炎细胞因子（IL-1 β、TNF-α）和IL-1受体拮抗剂的半定量RT-PCR。结果：与正常对照组相比，IBD患者的PMN分泌促炎细胞因子的量增加，同时检测到相应的mRNA。这一发现并非IBD的特异性，而是反映了一般的肠道炎症。IL-10显著抑制促炎细胞因子的分泌以及相应的mRNA concentration. Conclusions中性粒细胞是肠道炎症患者促炎细胞因子的重要来源，IL-10可以下调。
Background-Concentrations of pro-inflammatory cytokines are increased in the intestinal mucosa of patients with active inflammatory bowel disease (FED). Polymorphonuclear neutrophil granulocytes (PMN) are the most abundant cell type in intestinal lesions in IBD. Interleukin 10 (IL-IO) is an important contra-inflammatory cytokine which induces downregulation of pro-inflammatory cytokines.Aims-To investigate whether PMN from patients with UBD or infectious colitis, respectively, secrete increased amounts of pro-inflammatory cytokines and can be regulated try IL-10.Methods-Secretion (ELISA) as well as corresponding mRNA levels (semiquantitative RT-PCR) of pro-inflammatory cytokines (IL-1 beta, TNF-alpha) and of IL-l receptor antagonist were assessed in peripheral PMN. Results-PMN from patients with IBD are primed to secrete enhanced amounts of pro-inflammatory cytokines accompanied by detection of corresponding mRNAs in comparison with normal controls. This finding is not specific for IBD but rather reflects intestinal inflammation in general. IL-10 markedly inhibited proinflammatory cytokine secretion as well as corresponding mRNA concentrations.Conclusions-PMN are an important source of pro-inflammatory cytokines in patients with intestinal inflammation and can be downregulated by IL-10.