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Tetracycline suppresses ATPγS‐induced CXCL8 and CXCL1 production by the human dermal microvascular endothelial cell‐1 (HMEC‐1) cell line and primary human dermal microvascular endothelial cells
Author(s) -
Bender Anna,
Zapolanski Tamar,
Watkins Shan,
Khosraviani Ava,
Seiffert Kristina,
Ding Wanhong,
Wagner John A.,
Granstein Richard D.
Publication year - 2008
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2008.00716.x
Subject(s) - microbiology and biotechnology , endothelial stem cell , interleukin 8 , inflammation , chemokine , cell culture , cxcl1 , chemistry , biology , immunology , biochemistry , in vitro , genetics
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)γS, 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 ATPγS‐induced release of pro‐inflammatory mediators by HMEC‐1 cells and primary human dermal microvascular endothelial cells. TCN dose‐dependently inhibited ATPγS‐induced augmentation of CXCL8 (interleukin‐8) and CXCL1 (growth‐regulated oncogene‐α) production by HMEC‐1 cells and primary human dermal endothelial cells in vitro . TCN and ATPγS 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.