Abstract
The effects of moxifloxacin, a new methoxyfluoroquinolone, on the production of proinflammatory cytokines from human peripheral blood mononuclear cells (PBMCs) were evaluated. Moxifloxacin inhibited the production of tumor necrosis factor alpha (TNF-alpha) and/or interleukin-6 (IL-6) by PBMCs stimulated with lipopolysaccharide (LPS), lipoteichoic acid (LTA), and heat-killed bacteria in a concentration-dependent manner without cytotoxic effects. The addition of moxifloxacin reduced the population of cells positive for CD-14 and TNF-alpha and for CD-14 and IL-6 among the LPS- or LTA-stimulated PBMCs. By Western blot analysis, moxifloxacin pretreatment reduced the degradation of IkappaBalpha in LPS-stimulated PBMCs. In conclusion, moxifloxacin could interfere with NF-kappaB activation by inhibiting the degradation of IkappaBalpha and reduce the levels of production of proinflammatory cytokines.
MeSH terms
-
Adjuvants, Immunologic / pharmacology
-
Anti-Infective Agents / pharmacology*
-
Aza Compounds / pharmacology*
-
Blotting, Western
-
Ceftriaxone / pharmacology
-
Cell Survival
-
Cephalosporins / pharmacology
-
Cytokines / biosynthesis*
-
Enzyme-Linked Immunosorbent Assay
-
Escherichia coli / immunology
-
Flow Cytometry
-
Fluoroquinolones
-
Humans
-
I-kappa B Proteins / metabolism
-
In Vitro Techniques
-
Interleukin-6 / biosynthesis
-
Lipopolysaccharide Receptors / metabolism
-
Monocytes / drug effects*
-
Monocytes / metabolism*
-
Moxifloxacin
-
Ofloxacin / pharmacology
-
Quinolines / pharmacology*
-
Streptococcus pneumoniae / immunology
-
Tumor Necrosis Factor-alpha / biosynthesis
Substances
-
Adjuvants, Immunologic
-
Anti-Infective Agents
-
Aza Compounds
-
Cephalosporins
-
Cytokines
-
Fluoroquinolones
-
I-kappa B Proteins
-
Interleukin-6
-
Lipopolysaccharide Receptors
-
Quinolines
-
Tumor Necrosis Factor-alpha
-
Ceftriaxone
-
Ofloxacin
-
Moxifloxacin