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Effect of Macrolide Antibiotics on Human Endothelial Cells Activated byChlamydia pneumoniaeInfection and Tumor Necrosis Factor–α
Author(s) -
Silvia M. Uriarte,
Robert E. Molestina,
Richard D. Miller,
Jorge Guillermo Bernabó,
Alicia Farinati,
Kumiko Eiguchi,
Julio A. Ramírez,
James T. Summersgill
Publication year - 2002
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/340575
Subject(s) - roxithromycin , tumor necrosis factor alpha , monocyte , azithromycin , clarithromycin , microbiology and biotechnology , umbilical vein , antibiotics , protein synthesis inhibitor , chlamydia , interleukin 8 , macrolide antibiotics , immunology , antibacterial agent , cytokine , biology , medicine , in vitro , erythromycin , biochemistry
This study investigated the potential anti-inflammatory activity of 3 macrolide antibiotics, clarithromycin, roxithromycin, and azithromycin, in an in vitro model of transendothelial migration (TEM). Human umbilical vein endothelial cells (HUVECs) were seeded in Transwell inserts, treated with serial dilutions of the antibiotics, and infected with Chlamydia pneumoniae or stimulated with tumor necrosis factor (TNF)-alpha. In HUVECs infected with C. pneumoniae or stimulated with TNF-alpha, both azithromycin and roxithromycin caused significant decreases in neutrophil and monocyte TEM, compared with antibiotic-free controls. Clarithromycin had no detectable effect in either group. Azithromycin caused significant decreases in interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1, whereas roxithromycin significantly decreased IL-8. This study indicates heterogeneity in the anti-inflammatory activity of these antibiotics. Mechanisms of monocyte and neutrophil TEM inhibition by azithromycin and roxithromycin are unclear but may be partially due to inhibition of IL-8 and MCP-1 production.

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