|Hoang, K -|
|Saxton, A -|
|Lin, J -|
Submitted to: Campylobacter Helicobacter and Related Organisms International Workshop
Publication Type: Abstract Only
Publication Acceptance Date: August 14, 2009
Publication Date: September 27, 2009
Citation: Hoang, K.V., Stern, N.J., Saxton, A., Lin, J. 2009. Prevalence, development and molecular mechanisms of bacteriocin resistance in Campylobacter.. Campylobacter Helicobacter and Related Organisms International Workshop. Technical Abstract: In this study, susceptibilities of 137 C. jejuni and 20 C. coli isolates to two BCNs (OR-7 and E-760) were examined. Only one C. coli strain displayed resistance to the BCNs (MIC = 64 µg/ml) while others were susceptible with MIC ranging from 0.25 to 1 µg /ml. BCN-resistant (BCNR) C. coli mutant was also obtained by in vitro selection but no high-level BCNR mutants were selected. The BCN resistance in C. coli could be transferred to C. jejuni strains by natural transformation with frequency about 10-7 CFU/µg DNA/recipient cell. Using DNA microarray, we compared the transcriptome of a BCNR C. jejuni mutant with that of parent strain NCTC 11168. Microarray analysis revealed 9 genes were upregulated and 10 genes were downregulated more than two fold in the BCNR mutant. The majority of genes upregulated in the BCNR mutant encoded for zinc metallopeptidase, galactosyltransferase, and three different efflux pumps. Inactivation of these efflux pumps showed that only CmeABC efflux pump contributed Campylobacter resistance to the BCNs. Genomic examination of a 81-176-derived BCNR mutant using in vivo random transposon mutagenesis also indicated that CmeABC contributes C. jejuni to both intrinsic and acquired resistance to the BCNs.