J Bacteriol 2005, 187:304–319 PubMedCentralPubMedCrossRef 53 Hou

J Bacteriol 2005, 187:304–319.PubMedCentralPubMedCrossRef 53. House B, Kus JV, Prayitno N, Mair R, Que L, Chingcuanco F, Gannon V, Cvitkovitch DG, Barnett Foster D: Acid-stress-induced changes in enterohemorrhagic Escherichia coli O157:H7 virulence. Microbiol 2009,

155:2907–2918.CrossRef 54. Yin X, Wheatcroft R, Chambers JR, Liu B, Zhu J, Gyles CL: Contributions Epigenetics inhibitor of O-island 48 to adherence of Enterohemmorrhagic Escherichia coli O157:H7 to epithelial cells in vitro and in ligated pig ileal loops. Appl Environ Microbiol 2009, 75:5779–5786.PubMedCentralPubMedCrossRef 55. Dziva F, Mahajan A, Cameron R, Currie C, McKendrick , Wallis TS, Smith DGE, Stevens MP: EspP, a TypeV-secreted serine protease of enterohaemorrhagic Escherichia coli O157:H7, influences intestinal colonization of calves and adherence to bovine primary intestinal epithelial cells. FEMS Microbiol Lett 2007, 271:258–264.PubMedCrossRef 56. McAllister TA, Bae HD, Jones GA, Cheng KJ: Microbial attachment and feed digestion in the rumen. J Anim Sci 1994, 72:3004–3018.PubMed Competing interests The authors HSP inhibitor declare no competing financial interests. Authors’ contributions ITK was the project leader and designed, coordinated, conducted experiments, analyzed results, interpreted

data and drafted the manuscript. TBS assisted in design of experiments, VFA analysis, interpreted results and contributed to the final draft of the manuscript. JDL conducted iTRAQ proteomics, verified data generated

and contributed to the final draft of the manuscript. All authors read and approved the final manuscript.”
“Background Diflunisal Haemophilus influenzae is a γ-Proteobacterium from within the order the Pasteurellacae. It is an obligate human commensal of the nasopharynx and in most cases it remains as a commensal but some strains can transit from the nasopharynx to other parts of the body and in doing so cause numerous types of disease [1]. There are strain-specific factors that enable pathogenic strains to transit to, and then survive within, different parts of the body, where the stresses of multiple environmental conditions require a breadth of adaptive abilities that permit survival and growth [2]. There are a number of physical parameters that are known to vary between parts of the human host, including: oxygen tension, carbon/energy/nitrogen source, pH and the presence of reactive oxygen and reactive nitrogen species. Defence against these can be directly encoded through detoxification genetic pathways, but also through broader mechanisms for environmental adaptation. In addition to specific pathways that respond to and deal with each of the damaging physical or chemical stressors present within the various environments the bacteria may encounter, many bacteria have a capacity to switch their lifestyle such that these stresses no longer cause damage to their cell.

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