PMID- 15215106
OWN - NLM
STAT- MEDLINE
DCOM- 20040907
LR  - 20181130
IS  - 0066-4804 (Print)
IS  - 1098-6596 (Electronic)
IS  - 0066-4804 (Linking)
VI  - 48
IP  - 7
DP  - 2004 Jul
TI  - Effects of fluoroquinolones on the migration of human phagocytes through 
      Chlamydia pneumoniae-infected and tumor necrosis factor alpha-stimulated 
      endothelial cells.
PG  - 2538-43
AB  - 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.
FAU - Uriarte, Silvia M
AU  - Uriarte SM
AD  - Infectious Diseases Laboratory, Room 311, Instructional Building, 500 South 
      Preston St., University of Louisville, Louisville, KY 40292, USA.
FAU - Molestina, Robert E
AU  - Molestina RE
FAU - Miller, Richard D
AU  - Miller RD
FAU - Bernabo, Jorge
AU  - Bernabo J
FAU - Farinati, Alicia
AU  - Farinati A
FAU - Eiguchi, Kumiko
AU  - Eiguchi K
FAU - Ramirez, Julio A
AU  - Ramirez JA
FAU - Summersgill, James T
AU  - Summersgill JT
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Antimicrob Agents Chemother
JT  - Antimicrobial agents and chemotherapy
JID - 0315061
RN  - 0 (Anti-Infective Agents)
RN  - 0 (Aza Compounds)
RN  - 0 (Chemokines)
RN  - 0 (Fluoroquinolones)
RN  - 0 (Quinolines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 6GNT3Y5LMF (Levofloxacin)
RN  - A4P49JAZ9H (Ofloxacin)
RN  - L4618BD7KJ (Gatifloxacin)
RN  - U188XYD42P (Moxifloxacin)
SB  - IM
MH  - Anti-Infective Agents/*pharmacology
MH  - Aza Compounds/pharmacology
MH  - Cell Movement/drug effects
MH  - Chemokines/biosynthesis
MH  - *Chlamydia
MH  - Endothelial Cells/*cytology/drug effects
MH  - Fluoroquinolones/*pharmacology
MH  - Gatifloxacin
MH  - Humans
MH  - Levofloxacin
MH  - Monocytes/drug effects
MH  - Moxifloxacin
MH  - Neutrophils/drug effects
MH  - Ofloxacin/pharmacology
MH  - Phagocytes/*drug effects
MH  - Pneumonia, Bacterial/*pathology
MH  - Quinolines/pharmacology
MH  - Stimulation, Chemical
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Umbilical Veins/cytology/pathology
PMC - PMC434182
EDAT- 2004/06/25 05:00
MHDA- 2004/09/08 05:00
PMCR- 2004/07/01
CRDT- 2004/06/25 05:00
PHST- 2004/06/25 05:00 [pubmed]
PHST- 2004/09/08 05:00 [medline]
PHST- 2004/06/25 05:00 [entrez]
PHST- 2004/07/01 00:00 [pmc-release]
AID - 48/7/2538 [pii]
AID - 1002-03 [pii]
AID - 10.1128/AAC.48.7.2538-2543.2004 [doi]
PST - ppublish
SO  - Antimicrob Agents Chemother. 2004 Jul;48(7):2538-43. doi: 
      10.1128/AAC.48.7.2538-2543.2004.