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首页> 外文期刊>Experimental dermatology >Tetracycline suppresses ATP gamma S-induced CXCL8 and CXCL1 production by the human dermal microvascular endothelial cell-1 (HMEC-1) cell line and primary human dermal microvascular endothelial cells.
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Tetracycline suppresses ATP gamma S-induced CXCL8 and CXCL1 production by the human dermal microvascular endothelial cell-1 (HMEC-1) cell line and primary human dermal microvascular endothelial cells.

机译：四环素抑制人皮肤微血管内皮细胞1（HMEC-1）细胞系和原代人皮肤微血管内皮细胞对ATPγS诱导的CXCL8和CXCL1的产生。

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摘要

Tetracyclines (TCN) have powerful anti-inflammatory properties in addition to their anti-microbial effects. These anti-inflammatory effects are thought to play a role in inhibiting cutaneous inflammation in patients with rosacea and acne; however, the mechanism(s) of this action remains poorly understood. We have previously shown that adenosine-5'-triphosphate (ATP)gamma S, a hydrolysis-resistant ATP analogue, augments secretion of pro-inflammatory messengers by a human dermal microvascular endothelial cell line (HMEC-1). ATP released by the sympathetic nerves during stress may stimulate release of pro-inflammatory chemokines by dermal vessel endothelial cells, resulting in recruitment of inflammatory cells and exacerbation of inflammatory skin disease. Here we demonstrate that TCN inhibits ATP gamma S-induced release of pro-inflammatory mediators by HMEC-1 cells and primary human dermal microvascular endothelial cells. TCN dose-dependently inhibited ATP gamma S-induced augmentation of CXCL8 (interleukin-8) and CXCL1 (growth-regulated oncogene-alpha) production by HMEC-1 cells and primary human dermal endothelial cells in vitro. TCN and ATP gamma S did not affect HMEC-1 cell viability as determined by trypan-blue exclusion and cell counts. Inhibition of production of inflammatory mediators by endothelial cells may be one mechanism by which TCN improves inflammatory skin diseases. The ability to inhibit release of inflammatory mediators induced in HMEC-1 cells by purinergic agonists may be a useful way to screen for potential therapeutic agents for cutaneous inflammation.
机译：四环素（TCN）除具有抗微生物作用外，还具有强大的抗炎特性。这些抗炎作用被认为在抑制酒渣鼻和痤疮患者的皮肤炎症中发挥作用。但是，此动作的机制仍然知之甚少。先前我们已经表明，耐水解的ATP类似物5'-三磷酸腺苷（ATP）γS通过人类皮肤微血管内皮细胞系（HMEC-1）增强促炎信使的分泌。应激期间由交感神经释放的ATP可能刺激真皮血管内皮细胞释放促炎性趋化因子，从而导致炎症细胞募集并加剧炎症性皮肤病。在这里，我们证明了TCN通过HMEC-1细胞和原代人皮肤微血管内皮细胞抑制ATPγS诱导的促炎性介质释放。 TCN剂量依赖性地抑制了HMEC-1细胞和原代人皮肤内皮细胞在体外对ATPγS诱导的CXCL8（白介素8）和CXCL1（生长调节的癌基因α）产生的增强作用。通过台盼蓝排除法和细胞计数确定，TCN和ATPγS不会影响HMEC-1细胞的活力。内皮细胞抑制炎性介质的产生可能是TCN改善炎性皮肤疾病的一种机制。嘌呤能激动剂抑制HMEC-1细胞诱导的炎症介质释放的能力可能是筛选潜在的皮肤炎症治疗剂的有用方法。

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