| dc.description.abstract | Antibiotics are used widely today and large amounts of them used for human
therapy. When results in the selection occurred, bacteria resist to multiple drugs.
Multidrug resistance in bacteria is still not clear in some mechanisms, in which,
the increased expression of genes that code for multidrug efflux pumps extrudes
drugs in a wide range. This project investigate more on gene function
modification and molecular mechanisms involved in over expression that code
for multidrug efflux pumps in Pseudomonas aeruginosa (P. aeruginosa). The
selected object was a suspected mutated P. aeruginosa ATCC 9027. The
mutations, which were found as a result of serial exposures in P. aeruginosa
ATCC 9027 under Moxifloxacin Minimal Inhibitory Concentration (MOX-MIC),
were conjectured changes of genes molecular secreting over expression of
multidrug efflux pumps. In this study, mexR and nalC were characterized using
specific primers and by sequencing of PCR products. The expression of mexC,
mexD, oprJ (MexCD-OprJ) was assessed by RT-PCR for P. aeruginosa strains. In
this study, from RT-PCR results, overexpression in mexC and oprJ occurred. It is
proved that the involvement of a hypothetical insertion sequence (ISPAVy01) in
nfxB was able to lead to overexpression of mexC and oprJ in mexCD-oprJ operon
and seemed to play an important role in emergence of MOX-resistant as well as
MDR in P. aeruginosa.
Keywords:
Pseudomonas aeruginosa, Moxifloxacin, mexR, nalC, MexCD–oprJ | en_US |
