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Immunomodulatory effects of azithromycin on serum amyloid A production in lipopolysaccharide-induced endotoxemia in mice

Growing number of scientific investigations indicate that certain macrolides, a well-known group of antibiotics isolated from actinomycetes, also exert anti-inflammatory and immunomodulatory properties by modulating leukocyte function and circulating concentrations of proinflammatory cytokines. These macrolide properties have been employed in various chronic inflammatory disorders, such as diffuse panbronchiolitis, chronic obstructive pulmonary disease and cystic fibrosis. We have defined more precisely the immunomodulatory activity of azithromycin in LPS-induced endotoxemia. Azithromycin exerted anti-inflammatory activity by preventing the initial neutropenia and lymphopenia and in the later stage of the inflammatory reaction by inhibiting LPS-induced increase in blood neutrophil number. In healthy animals azithromycin increased the concentration of serum SAA. The same was observed at the induction phase of the inflammatory reaction when azithromycin increased LPS stimulated SAA synthesis, possibly by induction of plasma IL-6 secretion. In the later stage of inflammation azithromycin ameliorated LPS-induced increase in serum SAA concentration. Results presented indicate that azithromycin, administered at the beginning of LPS-induced endotoxemia, acts pro-inflammatory. On the other hand it tends to lessen the longer term severe increases in inflammatory mediators induced by LPS. These actions of azithromycin may provide additional therapeutic benefit in sepsis and also suggest potential new directions for inhibitors of inflammatory reactions in sepsis.

azithromycin anti-inflammatory activity; azithromycin immunomodulation; endotoxemia; IL6; LPS; serum amyloid A

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