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in Streptococcus pneumoniae . PLoS Pathog 2012, 8:e1002788.PubMedCrossRef 59. Ding Y, Davis BM, Waldor MK: Hfq is essential for Vibrio cholerae virulence and downregulates sigma expression. Mol Microbiol XL184 cell line 2004, 53:345–354.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions RJH conceived the study. All authors participated in the study design and data analysis. RJH performed the sequence alignment, primer extension

assay, in vitro growth assays, and drafted the manuscript. RJH and DJM performed the chinchilla experiments. RJH and TWS performed the infant rat studies. DJM, JQEZ5 nmr TWS, PWW and TLS revised the manuscript. All authors read and approved the final manuscript.”
“Background Campylobacter jejuni is a Gram-negative, spiral-shaped, motile bacterium and is a leading cause of bacterial food-borne enteritis in humans [1, 2]. Most human C. jejuni infections are acquired by consuming or handling contaminated poultry, milk or water. Clinical symptoms of campylobacteriosis Dichloromethane dehalogenase can range from mild diarrhea to fever, headache, abdominal cramping, vomiting and bloody diarrhea. Studies also demonstrated that Campylobacter infection is associated with

Guillain-Barré syndrome as a post-infection complication [3]. Although most campylobacteriosis cases are self-limiting, antibiotic therapy may be necessary for severe or persistent illness [4]. Macrolide, such as erythromycin (Ery), is the drug of choice for treating campylobacteriosis, but the frequency of resistance to this class of antibiotic is selleck screening library rising [5, 6]. As an inhibitor of protein translation in bacterial cells, Ery and other macrolide antibiotics interfere with aminoacyl translocation, preventing the transfer of the tRNA bound at the A site to the P site of the rRNA complex. Without this translocation, the A site remains occupied and thus precludes the incoming tRNA from attaching its amino acid to the nascent polypeptide [7–9]. The molecular mechanism of resistance to Ery in C. jejuni has been extensively studied and is conferred largely by target modification (such as mutations in the 23S rRNA gene and ribosomal proteins) [6, 7, 10] and antibiotic efflux pumps [11].