Particulate matter initiates inflammatory cytokine release by activation of capsaicin and acid receptors in a human bronchial epithelial cell line.
Particulate matter initiates inflammatory cytokine release by activation of capsaicin and acid receptors in a human bronchial epithelial cell line.
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颗粒物质通过激活人支气管上皮细胞系中的辣椒素和酸性受体来启动炎症细胞因子的释放。
DOI：
10.1006/taap.1998.8567
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发表时间：
1999
影响因子：
3.8
通讯作者：
Robert B. Devlin
中科院分区：
文献类型：
--
作者：
Bellina Veronesi;M. Oortgiesen;J. Carter;Robert B. Devlin
最近的实验表明，人的支气管上皮细胞(即BEAS-2B)在神经肽、P物质(SP)、降钙素基因相关蛋白(CGRP)和植物刺激物辣椒素原型的作用下，以受体介导的方式释放促炎细胞因子(即IL-6和TNFpha)。在目前的实验中，我们研究了这些受体与颗粒物(PM)相关的细胞炎症的相关性。BEAS-2B细胞暴露于残留的石油飞灰颗粒(ROFA)后，细胞内钙离子浓度([Ca~(2+)]_i)在暴露后即刻升高，关键炎症细胞因子转录产物(IL-6、IL-8、TNFα)在暴露后2 h内升高，4 h后释放IL-6和IL-8细胞因子蛋白。用选择SP或CGRP受体的药物拮抗剂预处理BEAS-2B细胞，可使ROFA刺激的IL-6细胞因子的产生分别减少约25%和50%。然而，辣椒素(即香草素)受体拮抗剂卡萨西平(CPZ)可抑制细胞内即刻[Ca~(2+)]i升高、转录水平降低(即IL-6、IL-8、TNFα)，并使IL-6细胞因子释放减少至对照水平。无钙条件下，ROFA作用于BEAS-2B细胞后，细胞内[Ca~(2+)]i无明显增加，细胞因子转录水平(即IL-6、IL-8、TNFα)和IL-6释放水平降低，提示ROFA刺激的细胞因子的形成部分依赖于细胞外钙源。最后一组实验比较了ROFA的可溶组分和酸性不溶组分的炎症特性。暴露于ROFA或通过0.2微米孔过滤器过滤的ROFA的BEAS-2B细胞产生模棱两可的IL-6。BEAS-2B细胞在pH 5.0条件下作用15min，4h后释放适量的IL-6。这种细胞因子的释放可以被pH受体拮抗剂阿米洛利阻断，但不能被CPZ阻断。在ROFA暴露前用阿米洛利预处理的BEAS-2B细胞显示出IL-6的部分(约25%)减少。综上所述，这些数据表明，ROFA的酸性、可溶性成分通过激活辣椒素和pH敏感的刺激受体，启动BEAS-2B细胞中细胞因子的释放。
Recent experiments have shown that human bronchial epithelial cells (i.e., BEAS-2B) release pro-inflammatory cytokines (i.e., IL-6 and TNFalpha) in a receptor-mediated fashion in response to the neuropeptides, substance P (SP), calcitonin gene-related protein (CGRP), and the prototype botanical irritant capsaicin. In the present experiments, we examined the relevance of these receptors to particulate matter (PM)-associated cellular inflammation. BEAS-2B cells, exposed to residual oil fly ash particles (ROFA), responded with an immediate (<30 s) increase in intracellular calcium levels ([Ca2+]i), increases of key inflammatory cytokine transcripts (i.e., IL-6, IL-8, TNFalpha) within 2 h exposure, and subsequent release of IL-6 and IL-8 cytokine protein after 4 h exposure. Pretreatment of BEAS-2B cells with pharmacological antagonists selective for the SP or CGRP receptors reduced the ROFA-stimulated IL-6 cytokine production by approximately 25 and 50%, respectively. However, pretreatment of these cells with capsazepine (CPZ), an antagonist for capsaicin (i.e., vanilloid) receptors, inhibited the immediate increases in [Ca2+]i, diminished transcript (i.e., IL-6, IL-8, TNFalpha) levels and reduced IL-6 cytokine release to control levels. BEAS-2B cells exposed to ROFA in calcium-free media failed to demonstrate increases of [Ca2+]i and showed reduced levels of cytokine transcript (i.e., IL-6, IL-8, TNFalpha) and IL-6 release, suggesting that ROFA-stimulated cytokine formation was partially dependent on extracellular calcium sources. A final set of experiments compared the inflammatory properties of the soluble and acidic insoluble components of ROFA. BEAS-2B cells, exposed to ROFA or ROFA that had been filtered through a 0.2-micrometer pore filter, produced equivocal IL-6. BEAS-2B cells exposed to pH 5.0 media for 15 min released moderate amounts of IL-6, 4 h later. This cytokine release could be blocked by amiloride, a pH receptor antagonist, but not by CPZ. BEAS-2B cells, pretreated with amiloride before ROFA exposure, showed a partial (approximately 25%) reduction of IL-6. Together, these data indicate that the acidic, soluble components of ROFA initiate cytokine release in BEAS-2B cells through activation of both capsaicin- and pH-sensitive irritant receptors.
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DOI：
--
发表时间：
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期刊：
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DOI：
10.1073/pnas.91.3.947
发表时间：
1994-02-01
影响因子：
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DOI：
--
发表时间：
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期刊：
Journal of exposure analysis and environmental epidemiology.
影响因子：
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作者：
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通讯作者：
Thurston,GD
影响因子：
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作者：
Lisa Pierce;F. Alessandrini;J. Godleski;J. Paulauskis
通讯作者：
Lisa Pierce;F. Alessandrini;J. Godleski;J. Paulauskis