Colistin resistance inPseudomonas aeruginosathat is not linked toarnB. Issue 6 (June 2017)

• Record Type: Journal Article
• Authors: Chung, Eun Seon; Lee, Ji‐Young; Rhee, Ji‐Young; Ko, Kwan Soo
• Is Part Of: Journal of medical microbiology. Volume 66:Issue 6(2017)
• Publication Date: 2017-06
• Subjects: arnB -- colistin -- lipid A; Medical microbiology -- Periodicals; 616.9041
• DOI: 10.1099/jmm.0.000456
• Languages: English
• ISSNs: 0022-2615

Abstract

Abstract : Purpose. : It is known that the arnB (or pmrH ) gene encoding uridine 5′‐(beta‐1‐threo‐pentapyranosyl‐4‐ulose diphosphate) aminotransferase plays a critical role in colistin resistance in Pseudomonas aeruginosa through the addition of 4‐amino‐4‐deoxy‐l‐arabinose (l‐Ara4N) to lipid A. In this study, we attempted to obtain a colistin‐resistant mutant from an arnB ‐deleted mutant through exposure to colistin. Methodology. : We constructed an arnB deletion mutant (P5Δ arnB :: nptIII ) from a colistin‐susceptible strain (P5) by allelic replacement mutagenesis, and colistin‐resistant mutants were selected in vitro using P5 and P5Δ arnB :: nptIII . The growth rate, lipid A structure, biofilm‐forming activity and cell viability in diverse stressful conditions (osmotic, oxidative, acidic and heat stress) were investigated. Expression of phoP, pmrA, parR, and cprR was evaluated by qRT‐PCR. Results. : An arnB deletion mutant was shown to develop colistin resistance through the addition of l‐Ara4N to lipid A, despite a low survival rate (over 1000‐fold lower than that of the wild‐type strain) in the media with colistin. Two colistin‐resistant mutants showed higher survival rates than colistin‐susceptible strains against 5% NaCl. In the presence of acidic and heat stress, P5Δ arnB :: nptIII ‐Cst R exhibited higher survival rates during conditions of 1% HCl and 42 °C than the other strains. Both phoP and pmrA genes were overexpressed significantly in both colistin‐resistant mutants, but parR and cprR genes were not. Conclusion. : We revealed that colistin resistance could be developed despite arnB deletion in P. aeruginosa through the addition of l‐Ara4N to lipid A, which was accompanied by diverse physiological changes.