Secretion of interleukin-8 by human-derived cell lines infected with Mycobacterium bovis.
Secretion of interleukin-8 by human-derived cell lines infected with Mycobacterium bovis.
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DOI：
10.1080/09629350410001664743
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发表时间：
2004-02
影响因子：
4.6
通讯作者：
García-Martínez E
中科院分区：
文献类型：
--
作者：
Méndez-Samperio P;Palma-Barrios J;Vázquez-Hernández A;García-Martínez E
背景：卡介苗(BCG)在预防人类结核病方面的不同功效促使人们探索卡介苗诱导趋化因子的机制。在这项研究中，我们的实验旨在确定转录因子核因子-kappaB(NF-kappaB)和细胞内钙在人源性单核细胞系U937和感染卡介苗的人上皮细胞系Hep-2产生白细胞介素8(IL-8)中的作用。方法：采用酶联免疫吸附试验检测卡介苗感染U937细胞和Hep-2细胞培养上清液中IL-8的浓度。我们用柳氮磺胺吡啶和姜黄素这两种广为人知的核因子-kappaB活性抑制剂，用乙二胺四乙酸去除细胞外的钙离子，或用细胞通透剂1，2-双(2-氨基苯氧基)乙烷-N，N，N‘，N’-四乙酸四乙酰氧甲基酯来螯合细胞内可释放的钙离子储备，以探讨卡介苗诱导IL-8分泌的机制。结果：酶联免疫吸附试验显示感染牛分枝杆菌的细胞株IL-8蛋白分泌增加。这一效应在统计学上具有显著意义(p<；0.01)。当抑制牛分枝杆菌感染细胞的钙内流时，IL-8的分泌也受到抑制。值得注意的是，核因子-kappaB的特异性抑制剂(柳氮磺胺吡啶和姜黄素)抑制牛分枝杆菌诱导的U937细胞或Hep-2细胞分泌IL-8。结论：上述结果表明，在牛分枝杆菌诱导单核细胞或上皮细胞分泌IL-8过程中，核因子-kappaB的激活是一个重要的信号转导途径。此外，结果表明，钙离子内流对感染牛分支杆菌的U937细胞和Hep-2细胞的IL-8分泌有直接影响。
BACKGROUND: The variable efficacy of bacillus Calmette-Guérin (Mycobacterium bovis BCG) in protecting humans against tuberculosis has prompted a search for the mechanisms through which BCG induces chemokines. In this study, our experiments were designed to determine the role of the transcription factor nuclear factor-kappaB (NF-kappaB) and intracellular calcium in the production of interleukin (IL)-8, a main chemotactic factor, by human-derived monocytic cell line U937 and by a human epithelial HEp-2 cell line infected with M. bovis BCG. METHODS: The concentrations of IL-8 in culture supernatants of U937 cells or HEp-2 cells infected with M. bovis BCG were determined by enzyme-linked immunosorbent assay. We used sulfasalazine and curcumin, which are well-described inhibitors of NF-kappaB activity, and we used ethylenediamine tetraacetic acid to deplete extracellular Ca2+ or used the cell-permeable agent 1,2-bis (2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetra (acetoxymethyl) ester to chelate releasable intracellular stores of Ca2+ in order to investigate the mechanisms through which M. bovis BCG induces IL-8 secretion in our system. RESULTS: The enzyme-linked immunosorbent assay showed that IL-8 protein secretion was elevated in M. bovis-infected cell lines. This effect was statistically significant (p < 0.01). When calcium influx was suppressed in M. bovis-infected cell lines, IL-8 secretion was inhibited. Notably, specific inhibitors of NF-kappaB (sulfasalazine and curcumin) inhibited M. bovis-induced IL-8 secretion from U937 cells or HEp-2 cells. CONCLUSIONS: Collectively, these results indicate that activation of NF-kappaB is an important signal transduction pathway in M. bovis-induced IL-8 secretion in monocytic or epithelial cells. Furthermore, the results showed that calcium influx had a direct effect on IL-8 secretion in U937 cells or HEp-2 cells infected with M. bovis.
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3.1
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Juffermans, NP;Verbon, A;van der Poll, T
通讯作者：
van der Poll, T
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