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meliloti . J Bacteriol 2007,189(19):7077–7088.PubMedCentralPubMedCrossRef 50. Krol E, Becker A: Global transcriptional analysis of the phosphate starvation response in Sinorhizobium meliloti strains 1021 and 2011. Mol Genet Genomics 2004,272(1):1–17.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MJT and MJD conceived of the study. MJT and MIR carried out the phenotypic analyses of the E. meliloti denitrification mutants. TC and JJP participated in the gene expression experiments. MJD and EJB supported the research. MJT and MJD wrote the Adavosertib manuscript. EJB coordinated and critically revised Acesulfame Potassium the manuscript. All of the authors read and approved the manuscript.”
“Background Campylobacter jejuni (C. jejuni), a microaerophilic, spiral-shaped, flagellated Gram-negative bacterium, is the most frequent cause of human gastroenteritis worldwide [1]. C. jejuni infections are often caused by consumption of undercooked poultry, unpasteurised milk or contaminated water

[2]. Adhesion of C. jejuni to host cells plays an important role in colonisation of chickens and in human infection [3]. Campylobacter binding to host cell receptors is not mediated by fimbria or pili, like in E. coli and Salmonella[4]. As noted in a recent review, other bacterial cell structures may contribute to interaction of Campylobacter with host cells [5]. In some cases, bacterial adhesion can be mediated by oligosaccharides present on the surface of host cells [6, 7]. In other cases, it is a pathogen oligosaccharide that is responsible for binding to specific, lectin-like, host cell structures. For example, a pathogenic Gram-positive bacterial species Nocardia rubra binds to a human lectin (intelectin) expressed by cells in different organs including intestine [8].