Benzydamine inhibits the release of tumor necrosis factor-α and monocyte chemotactic protein-1 byCandida albicans-stimulated human peripheral blood cells

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Abstract

Benzydamine is a non-steroidal antiinflammatory drug, devoid of activity on arachidonic acid metabolism, which is extensively used as a topical drug in inflammatory conditions, particularly for the treatment of bacterial vaginosis andCandida albicans-sustained vaginitis. In the present study the effects of benzydamine on the production of several inflammatory cytokines were examined in cultures ofCandida albicans-stimulated human mononuclear cells. Benzydamine (6.25-50 ΜM) inhibitedCandida-induced tumor necrosis factor-α and, to a lesser extent, interleukin-1 Β production, whereas it did not affect interleukin-6 release. Benzydamine also blocked monocyte chemotactic protein-1 secretion, but it did not affect interleukin-8 production. Unlike benzydamine, ibuprofen and naproxen, two non-steroidal antiinflammatory drugs also used topically, were unable to suppress inflammatory lymphokine production fromCandida-activated mononuclear cells. These data suggesrthat benzydamine may be effective in localCandida infections at least in part by suppressing inflammatory cytokine and monokine production in the vaginal mucosa and consequently decreasing their levels in vaginal secretions.