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J Infect Dis. 2011 Apr 15;203(8):1110-9. doi: 10.1093/infdis/jiq159. Epub 2011 Feb 28.

Rifampin protects human lung epithelial cells against cytotoxicity induced by clinical multi and pandrug-resistant Acinetobacter baumannii.

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Service of Infectious Diseases, Institute of Biomedicine of Seville (IBiS), University Hospital Virgen del Rocío/CSIC/University of Seville, Spain.



Recently, it has become apparent that rifampin can act on eukaryotic cells modulating production of host mediators. We aimed to study the cytoprotective effect of rifampin against multidrug- and pandrug-resistant Acinetobacter baumannii-induced cell death using human lung epithelial cells.


We pretreated A549 cells with rifampin and infected them with 3 different A. baumannii strains (susceptible, multidrug-resistant, and pandrug-resistant) that induce cell death. Cellular viability, apoptosis and host mediators, free radicals, and proinflammatory cytokines associated with A. baumannii pathogenesis were studied. Moreover, bacterial concentrations in A549 cells culture were determined.


Rifampin-pretreated A549 cells demonstrated decreases in apoptosis and cell death induced by A. baumannii. The oxidative stress and proinflammatory responses to A. baumannii were reduced in rifampin-pretreated A549 cells, as shown by decreased superoxide anion, tumor necrosis factor-α, and interleukin-6. Furthermore, bacterial count performed in A549 cell culture medium showed that rifampin did not reduce significantly the bacterial concentrations.


These data demonstrate that rifampin is able to attenuate the cellular damage induced by multidrug- and pandrug-resistant A. baumannii clinical isolates without being relevantly bactericidal. Indeed, the cytoprotective effect of rifampin was observed on the decrease of dead cells induced by A. baumannii by reducing oxidative stress and proinflammatory cytokines release.

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