Roles of lipooligosaccharide and capsular polysaccharide in antimicrobial resistance and natural transformation of Campylobacter jejuni.
OBJECTIVE
This study is aimed to determine the role of capsular polysaccharide (CPS) and lipooligosaccharide (LOS) in modulating antimicrobial resistance and natural transformation of Campylobacter jejuni, an important food-borne human pathogen.


METHODS
A series of C. jejuni mutants, which are defective in either CPS or LOS or both, were constructed. The antimicrobial susceptibility, bacterial surface hydrophobicity, natural transformation frequency and DNA binding and uptake were measured and compared between the mutants and the wild-type strain.


RESULTS
Truncation of LOS greatly reduced (8-fold) the intrinsic resistance of C. jejuni to erythromycin, a key antibiotic used for treating human campylobacteriosis, while the loss of CPS did not result in significant changes in the susceptibility to antimicrobial agents. Notably, mutation of LOS also significantly increased (>16-fold) the susceptibility to erythromycin in C. jejuni mutants carrying the A2074G mutation in 23S rRNA. The increased susceptibility to erythromycin in the LOS mutant was probably due to enhanced permeability to this antibiotic, because the LOS mutation rendered the surface of C. jejuni more hydrophobic. Loss of CPS and truncation of LOS increased the transformation frequency by 4- and 25-fold, respectively, and mutation of both CPS and LOS resulted in a 97-fold increase in the transformation frequency. Consistent with the increased transformation frequencies, the CPS and LOS mutants showed enhanced rates of DNA uptake.


CONCLUSIONS
These results demonstrate that the surface polysaccharides in C. jejuni contribute to the resistance to erythromycin, a clinically important antibiotic, but restrict natural transformation.
Jeon
Byeonghwa
B
Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, USA.
Muraoka
Wayne
W
Scupham
Alexandra
A
Zhang
Qijing
Q
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D016123:Campylobacter jejuni / Q000187:drug effects* / Q000502:physiology*; D004269:DNA, Bacterial / Q000378:metabolism; D024881:Drug Resistance, Bacterial; D004917:Erythromycin / Q000494:pharmacology; D006801:Humans; D008070:Lipopolysaccharides / Q000172:deficiency / Q000378:metabolism*; D009154:Mutation; D017354:Point Mutation; D011135:Polysaccharides, Bacterial / Q000235:genetics / Q000378:metabolism*; D012335:RNA, Ribosomal / Q000235:genetics; D017384:Sequence Deletion; D014169:Transformation, Bacterial
D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D008070:Lipopolysaccharides; D011135:Polysaccharides, Bacterial; D012335:RNA, Ribosomal; C023023:lipid-linked oligosaccharides; D004917:Erythromycin