Effects of Fluoroquinolones on the Migration of Human Phagocytes through Chlamydia pneumoniae-Infected and Tumor Necrosis Factor Alpha-Stimulated Endothelial Cells
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| Published in: | Antimicrobial Agents and Chemotherapy Vol. 48; no. 7; pp. 2538 - 2543 |
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| AbstractList | 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-alpha). 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-alpha, 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-alpha-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. 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-α). 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-α, 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-α-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. 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-α). 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-α, 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-α-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. Classifications Services AAC Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue AAC About AAC Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy AAC RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0066-4804 Online ISSN: 1098-6596 Copyright © 2014 by the American Society for Microbiology. For an alternate route to AAC .asm.org, visit: AAC 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- alpha ). 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- alpha , 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- alpha - 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 pruoroquinolone antibiotics are unknown but may be partially due to inhibition of IL-8 and MCP-1 production, respectively. |
| Author | Kumiko Eiguchi James T. Summersgill Jorge Bernabo Alicia Farinati Robert E. Molestina Richard D. Miller Silvia M. Uriarte Julio A. Ramirez |
| AuthorAffiliation | 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, Argentina 4 |
| AuthorAffiliation_xml | – name: 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, Argentina 4 |
| Author_xml | – sequence: 1 givenname: Silvia M surname: URIARTE fullname: URIARTE, Silvia M organization: Division of Infectious Diseases, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292, United States – sequence: 2 givenname: Robert E surname: MOLESTINA fullname: MOLESTINA, Robert E organization: Division of Infectious Diseases, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292, United States – sequence: 3 givenname: Richard D surname: MILLER fullname: MILLER, Richard D organization: Department of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, Kentucky 40292, United States – sequence: 4 givenname: Jorge surname: BERNABO fullname: BERNABO, Jorge organization: Department of Medicine, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina – sequence: 5 givenname: Alicia surname: FARINATI fullname: FARINATI, Alicia organization: Department of Microbiology and Immunology, University of Salvador, Buenos Aires, Argentina – sequence: 6 givenname: Kumiko surname: EIGUCHI fullname: EIGUCHI, Kumiko organization: Department of Microbiology and Immunology, University of Salvador, Buenos Aires, Argentina – sequence: 7 givenname: Julio A surname: RAMIREZ fullname: RAMIREZ, Julio A organization: Division of Infectious Diseases, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292, United States – sequence: 8 givenname: James T surname: SUMMERSGILL fullname: SUMMERSGILL, James T organization: Division of Infectious Diseases, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292, United States |
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| Keywords | Human Levofloxacin Endothelial cell Chlamydia pneumoniae Chlamydiaceae Migration Moxifloxacin Infection Fluoroquinolone derivatives Gatifloxacin Chlamydiales Bacteria Antibacterial agent Quinolone derivatives Tumor necrosis factor α Phagocyte |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Corresponding author. Mailing address: Infectious Diseases Laboratory, Room 311, Instructional Building, 500 South Preston St., University of Louisville, Louisville, KY 40292. Phone: (502) 852-5132. Fax: (502) 852-1512. E-mail: j.summersgill@louisville.edu. Present address: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY 40536. |
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Reddit... The anti-inflammatory activities of three quinolones, levofloxacin, moxifloxacin, and gatifloxacin, were investigated with an in vitro model of... |
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| StartPage | 2538 |
| SubjectTerms | Anti-Infective Agents Anti-Infective Agents - pharmacology Antibacterial agents Antibiotics. Antiinfectious agents. Antiparasitic agents Aza Compounds - pharmacology Biologic Response Modifiers Biological and medical sciences Cell Movement - drug effects Chemokines - biosynthesis Chlamydia Chlamydia pneumoniae Endothelial Cells Endothelial Cells - cytology Endothelial Cells - drug effects Fluoroquinolones Fluoroquinolones - pharmacology Humans Levofloxacin Medical sciences Monocytes - drug effects Neutrophils - drug effects Ofloxacin - pharmacology Phagocytes Phagocytes - drug effects Pharmacology. Drug treatments Pneumonia, Bacterial Pneumonia, Bacterial - pathology Quinolines - pharmacology Stimulation, Chemical Tumor Necrosis Factor-alpha Tumor Necrosis Factor-alpha - pharmacology Umbilical Veins - cytology Umbilical Veins - pathology |
| Title | Effects of Fluoroquinolones on the Migration of Human Phagocytes through Chlamydia pneumoniae-Infected and Tumor Necrosis Factor Alpha-Stimulated Endothelial Cells |
| URI | http://aac.asm.org/content/48/7/2538.abstract https://www.ncbi.nlm.nih.gov/pubmed/15215106 https://journals.asm.org/doi/10.1128/AAC.48.7.2538-2543.2004 https://search.proquest.com/docview/17710158 https://search.proquest.com/docview/66647144 https://pubmed.ncbi.nlm.nih.gov/PMC434182 |
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