This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Uriarte, S. M. Articles by Summersgill, J. T. Search for Related Content PubMed PubMed Citation Articles by Uriarte, S. M. Articles by Summersgill, J. T.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, July 2004, p. 2538-2543, Vol. 48, No. 7
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.7.2538-2543.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Effects of Fluoroquinolones on the Migration of Human Phagocytes through Chlamydia pneumoniae-Infected and Tumor Necrosis Factor Alpha-Stimulated Endothelial Cells

Silvia M. Uriarte,¹ Robert E. Molestina,^1, Richard D. Miller,² Jorge Bernabo,³ Alicia Farinati,⁴ Kumiko Eiguchi,⁴ Julio A. Ramirez,¹ and James T. Summersgill^1,2*

Division of Infectious Diseases, Department of Medicine,¹ Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky 40292,² Department of Medicine, School of Medicine, University of Buenos Aires,³ Department of Microbiology and Immunology, University of Salvador, Buenos Aires, Argentina⁴

Received 25 September 2003/ Returned for modification 7 December 2003/ Accepted 4 March 2004

The anti-inflammatory activities of three quinolones, levofloxacin, moxifloxacin, and gatifloxacin, were investigated with an in vitro model of transendothelial migration (TEM). Human umbilical vein endothelial cells (HUVEC) were seeded in Transwell inserts, treated with serial dilutions of antibiotics, infected with Chlamydia pneumoniae, or stimulated with tumor necrosis factor alpha (TNF-). Neutrophils or monocytes were also preincubated with serial dilutions of each antibiotic. TEM was assessed by light microscopic examination of the underside of the polycarbonate membrane, and levels of interleukin-8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) were measured by enzyme-linked immunosorbent assay. In HUVEC infected with C. pneumoniae or stimulated with TNF-, all fluoroquinolones significantly decreased neutrophil and monocyte TEM, compared to antibiotic-free controls. Moxifloxacin and gatifloxacin produced a significant decrease in IL-8 in C. pneumoniae-infected and TNF--stimulated HUVEC; however, moxifloxacin was the only fluoroquinolone that produced a significant decrease in MCP-1 levels under both conditions. Results from this study indicate similarities in the anti-inflammatory activities of these fluoroquinolones, although no statistically significant decrease in chemokine secretion was observed when levofloxacin was used. Mechanisms of neutrophil and monocyte TEM inhibition by fluoroquinolone antibiotics are unknown but may be partially due to inhibition of IL-8 and MCP-1 production, respectively.

Present address: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536.

This article has been cited by other articles:

• Shalit, I., Halperin, D., Haite, D., Levitov, A., Romano, J., Osherov, N., Fabian, I. (2006). Anti-inflammatory effects of moxifloxacin on IL-8, IL-1{beta} and TNF-{alpha} secretion and NF{kappa}B and MAP-kinase activation in human monocytes stimulated with Aspergillus fumigatus. J Antimicrob Chemother 57: 230-235 [Abstract] [Full Text]