Effect of Antibiotics on the Generation of Reactive Oxygen Species

Yoshioka, Akira; Imamura, Sadao; Niwa, Yukie

doi:10.1111/1523-1747.ep12285793

Cited by 175 publications

(95 citation statements)

References 32 publications

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“…ROS have long been considered to be toxic and implicated in defense systems against infection (Miyachi et al, 1986;Schirmer et al, 1987). Recently, however, NADPH-oxidase (Nox) has received a lot of interest as source of ROS in cellular signaling and these Nox-derived ROS are suggested to act as specific signaling mediators in various non-phagocytic cells (Vaquero et al, 2004;Adachi et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

TNF-α-induced up-regulation of intercellular adhesion molecule-1 is regulated by a Rac-ROS-dependent cascade in human airway epithelial cells

et al. 2008

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Up-regulation of intercellular adhesion molecule-1 (ICAM-1) in the lung airway epithelium is associated with the epithelium-leukocyte interaction, critical for the pathogenesis of various lung airway inflammatory diseases such as asthma. However, little is known about how ICAM-1 is up-regulated in human airway epithelial cells. In this study, we show that tumor TNF-α induces monocyte adhesion to A549 human lung airway epithelium and also up-regulation of ICAM-1 expression. These effects were significantly diminished by pre-treatment with diphenyliodonium (DPI), an inhibitor of NADPH oxidase-like flavoenzyme. In addition, the level of reactive oxygen species (ROS) was increased in response to TNF-α in A549 cells, suggesting a potential role of ROS in the TNF-α-induced signaling to ICAM-1 expression and monocyte adhesion to airway epithelium. Further, we found out that expression of Rac

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Section: Discussionmentioning

confidence: 99%

TNF-α-induced up-regulation of intercellular adhesion molecule-1 is regulated by a Rac-ROS-dependent cascade in human airway epithelial cells

et al. 2008

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“…In addition, it is hypothesized that this high concentration of EM within the neutrophil cytoplasm may modulate neutrophil functions. In fact, EM-mediated inhibition of neutrophil chemotaxis (9,27,29,31,32), oxidant generation (1,13,27), and phagocytosis (27) have been reported. In addition, EM also shortens neutrophil survival by accelerating apoptosis (2).…”

Section: Methodsmentioning

confidence: 99%

Effect of Macrolide Antibiotics on Macrophage Functions

Fujita

Negayama

et al. 1996

Microbiology and Immunology

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Macrolide antibiotics have a variety of actions other than antimicrobial activities. Recently, it has been suggested that macrolide antibiotics act as immunomodulators.In this study, we evaluated the effects of macrolide antibiotics on macrophage functions.For the macrophage, we used the mouse macrophage cell line J774.1. The following effects of macrolide antibiotics on macrophage functions were evaluated: the effect of macrolide antibiotics on macrophage growth; the phagocytosis of beads; cytocidal activity against Candida albicans; and chemotaxis to lipopolysaccharide (LPS). Macrolide antibiotics except for azithromycin significantly stimulated the growth of the macrophage. In addition, pretreatment with macrolide antibiotics except for roxithromycin significantly stimulated the macrophage phagocytosis of beads, macrophage chemotaxis to LPS, and macrophage cytocidal activity against Candida albicans. These results suggest that macrolide antibiotics stimulate macrophage functions. There is increasing evidence that long-term administration of the macrolide antibiotic erythromycin (EM) is effective in the treatment of chronic respiratory infections, probably through actions other than its antimicrobial properties (19). Although the mechanism of the efficacy is uncertain, several hypotheses have been proposed, such as the immunomodulatory action of macrolide antibiotics. Macrolide antibiotics modulate the functions of inflammatory cells such as polymorphonuclear leukocytes, lymphocytes and macrophages (1, 33). In addition, macrolide antibiotics directly affect airway secretory cell (12) and epithelial cell (35) functions. These effects are proposed to explain the efficacy of macrolides in the treatment of inflammatory airway diseases. Several studies have been conducted concerning the interaction between phagocytic cells and macrolide antibiotics. However, there are few reports that evaluate the interaction between macrophage functions and several macrolide antibiotics. With this background, we evaluated various aspects of the interaction between four macrolide antibiotics and macrophages. These studies included the effect on growth, effect on phagocytic activity, effect on chemotaxis to lipopolysaccharide (LPS), and effect of cytotoxicity against Candida albicans. Materials and MethodsMacrophage. We used a murine macrophage cell line, J774.1. This cell line was obtained from the RIKEN Cell Bank (Ibaraki, Japan). This cell line was cultured in RPMI-1640 medium with 10% fetal bovine serum (FBS).Antibiotics. The EM (Japan Dynabot Co., Tokyo), clarithromycin (CAM, Japan Dynabot Co.), roxithromycin (RXM, Roussel Uclaf, Paris, France), and azithromycin (AZM, Pfizer Pharmaceuticals Inc., Japan) were provided by the respective manufacturers. These 4 drugs were dissolved in 90% methanol at a concentration of 2 mg/ml as a stock solution; then diluted with RPMI-1640 medium with 10% FBS. Several final concentrations of macrolide antibiotics (4 concentrations of each antibiotic) were used in the following experimen...

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“…These include: xanthine oxidase (Miyachi et al 1986;Satoh et al 1998;Fleming et al 2001), NADPH oxidase (Meyer et al 1999;Hohler et al 2000;Barry-Lane et al 2001;Beswick et al 2001;Seno et al 2001;Brandes et al 2002;Li et al 2002;Lassegue et al 2003;Parinandi et al 2003), and uncoupled NOS (Beretta et al 2003;Landmesser et al 2003). NADPH oxidase and uncoupled NOS are thought to be major…”

Section: Sources Of Reactive Oxygen Speciesmentioning

confidence: 99%