Effect of moxifloxacin on secretion of cytokines by human monocytes stimulated with lipopolysaccharide

Objective To determine the effect of moxifloxacin on secretion of cytokines by human monocytes stimulated with lipopolysaccharide (LPS) or Pansorbin. Methods Monocytes obtained from 10 healthy volunteer donors were stimulated with LPS or Pansorbin and exposed or not to different concentrations of th...

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Bibliographic Details
Published inClinical microbiology and infection Vol. 8; no. 1; pp. 26 - 30
Main Authors Araujo, F.G., Slifer, T.L., Remington, J.S.
Format Journal Article
LanguageEnglish
Published Oxford, UK Elsevier Ltd 01.01.2002
Blackwell Science, Ltd
Blackwell
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Summary:Objective To determine the effect of moxifloxacin on secretion of cytokines by human monocytes stimulated with lipopolysaccharide (LPS) or Pansorbin. Methods Monocytes obtained from 10 healthy volunteer donors were stimulated with LPS or Pansorbin and exposed or not to different concentrations of the fluoroquinolone antibiotic moxifloxacin. At 3, 6 and 24 h, the amounts of interleukin-1α (IL-1α), IL-1β, IL-6, IL-10, IL-12 (p70) and tumour necrosis factor-α (TNF-α) were measured in the supernatants of the monocyte cultures using enzyme-linked immunosorbent assay. Results Stimulation of human monocytes with either LPS or Pansorbin resulted in a significant increase in secretion of each of the cytokines examined. Treatment of LPS-stimulated monocytes with moxifloxacin significantly inhibited (P<0.01) secretion of IL-1α by monocytes of each of 10 human donors; the secretion of TNF-α was significantly inhibited (P<0.01) in monocytes from six of 10 donors. In general there was a trend towards inhibition of secretion of IL-6, IL-10 and IL-12 (p70), but the inhibitory effect was not statistically significant. Secretion of cytokines by Pansorbin-stimulated monocytes was not significantly inhibited by moxifloxacin. Conclusions Moxifloxacin has immunomodulatory activity through its capacity to alter the secretion of IL-1α and TNF-α by human monocytes.
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ISSN:1198-743X
1469-0691
DOI:10.1046/j.1469-0691.2002.00374.x