作者: Xiaoyuan He , Mingfeng Zhao , Jinyan Chen , Rimao Wu , Jianlei Zhang
DOI: 10.1371/JOURNAL.PONE.0136185
关键词:
摘要: Objective To study the main molecular mechanisms responsible for itraconazole resistance in clinical isolates of Candida krusei. Methods The 14α-demethylases encoded by ERG11 gene 16 C.krusei were amplified polymerase chain reaction (PCR), and their nucleotide sequences determined to detect point mutations. Meanwhile, efflux transporters (ABC1 ABC2) genes quantitative real-time reverse transcription (qRT-PCR) expression itraconazole-resistant (R), itraconazole-susceptible dose dependent (SDD) (S) at mRNA level. Results We found 7-point mutations all isolates, including 6 synonymous 1 missense mutation (C44T). However, was three groups. The levels showed higher compared with ones (P = 0.015 P 0.002 respectively). ABC2 group significantly than other two groups, appeared increase decrease susceptibility 0.007 SDD S, 0.016 R, P<0.001 S R While ABC1 presented lower resistant strains. ERG11, a (CK10) both voriconazole expressed highest isolates. Conclusions There are polymorphisms C.krusei. may not be involved development overexpression might acquired these isolates.