The anti-inflammatory drug Diclofenac retains anti-listerial activity in vivo.

AIMS

The interactions between nonsteroidal anti-inflammatory drugs (NSAID) and Listeria monocytogenes have not been sufficiently documented to date. The aim of this study was to investigate the possible effects of Diclofenac (Dc) in a murine listerial infection model.

METHODS AND RESULTS

Dc was administered orally at 2.5 mug g(-1) to female albino strain of laboratory mouse (BALB/c) thrice postinfection (1 x 10(8) CFU ml(-1) oral challenge with L. monocytogenes ATCC 51774), which resulted in significantly (P < 0.01) reduced bacterial counts in liver and spleen, decreased (10-fold, P < 0.05) hepatic colonization and necrosis, and caused up-regulation of the expression of inflammatory cytokines (interferon-gamma, interleukin-1beta, tumour necrosis factor-alpha), compared with drug-free control.

CONCLUSIONS

Dc may be useful as a promising adjuvant to the existing therapies in controlling systemic listerial infection. Further, quantitative structure-activity relationship studies might contribute in manipulating it as a lead compound for the synthesis of new, more effective nonantibiotics, perhaps, devoid of side-effects that could be recommended as a compassionate therapy for listeriosis.

SIGNIFICANCE AND IMPACT OF THE STUDY

This is the first in vivo study designed to evaluate the antilisterial effect of the NSAID Dc with special emphasis on the immunological mechanism of action of the drug.