Bacterial lipopolysaccharide confers resistance to G418, doxorubicin and taxol in the murine macrophage cell line, RAW264

Sweet, M. J. and Hume, D. A. (1996) Bacterial lipopolysaccharide confers resistance to G418, doxorubicin and taxol in the murine macrophage cell line, RAW264. Journal of Leukocyte Biology, 59 2: 280-286.

Author Sweet, M. J.
Hume, D. A.
Title Bacterial lipopolysaccharide confers resistance to G418, doxorubicin and taxol in the murine macrophage cell line, RAW264
Journal name Journal of Leukocyte Biology   Check publisher's open access policy
ISSN 0741-5400
Publication date 1996
Sub-type Article (original research)
Volume 59
Issue 2
Start page 280
End page 286
Total pages 7
Language eng
Abstract Many bacterial pathogens including Salmonella and Listeria replicate within macrophages. The susceptibility of these organisms to various antibiotics is dependent on the ability of macrophages to take up, retain, and deliver the antibiotic to the correct intracellular compartment. In this context, macrophages are known to express proteins that are involved in efflux of antibiotics and cytotoxic drugs, thereby reducing intracellular accumulation of such compounds. In our studies on the action of bacterial lipopolysaccharide (LPS) on the macrophage-like cell line, RAW264 we found that LPS treatment of these cells conferred resistance to the neomycin-related aminoglycoside G418 (geneticin). This phenotype was stable and was specific to LPS since colony-stimulating factor 1 and phorbol myristate acetate had no effect on G418 resistance. We have extended this observation to show that LPS induces transient resistance to the cytotoxic drugs taxol and doxorubicin. Macrophage resistance to cytotoxic drugs and antibiotics may have a number of important clinical consequences.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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Created: Tue, 11 Oct 2011, 14:02:37 EST by Matt Sweet on behalf of School of Chemistry & Molecular Biosciences