{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T05:20:41Z","timestamp":1761196841975},"reference-count":49,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2008,3,13]],"date-time":"2008-03-13T00:00:00Z","timestamp":1205366400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> Tetracyclines (TCN) have powerful anti\u2010inflammatory properties in addition to their anti\u2010microbial effects. These anti\u2010inflammatory 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\u20105\u2032\u2010triphosphate (ATP)\u03b3S, a hydrolysis\u2010resistant ATP analogue, augments secretion of pro\u2010inflammatory messengers by a human dermal microvascular endothelial cell line (HMEC\u20101). ATP released by the sympathetic nerves during stress may stimulate release of pro\u2010inflammatory 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\u03b3S\u2010induced release of pro\u2010inflammatory mediators by HMEC\u20101 cells and primary human dermal microvascular endothelial cells. TCN dose\u2010dependently inhibited ATP\u03b3S\u2010induced augmentation of CXCL8 (interleukin\u20108) and CXCL1 (growth\u2010regulated oncogene\u2010\u03b1) production by HMEC\u20101 cells and primary human dermal endothelial cells <jats:italic>in vitro<\/jats:italic>. TCN and ATP\u03b3S did not affect HMEC\u20101 cell viability as determined by trypan\u2010blue 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\u20101 cells by purinergic agonists may be a useful way to screen for potential therapeutic agents for cutaneous inflammation.<\/jats:p>","DOI":"10.1111\/j.1600-0625.2008.00716.x","type":"journal-article","created":{"date-parts":[[2008,3,13]],"date-time":"2008-03-13T07:39:51Z","timestamp":1205393991000},"page":"752-760","source":"Crossref","is-referenced-by-count":28,"title":["Tetracycline suppresses ATP\u03b3S\u2010induced CXCL8 and CXCL1 production by the human dermal microvascular endothelial cell\u20101 (HMEC\u20101) cell line and primary human dermal microvascular endothelial 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