jejuni during slaughter can contaminate cooling water, knives and

jejuni during slaughter can contaminate cooling water, knives and poultry meat in the processing plant [4]. During transmission of C. jejuni from animals, primarily poultry, to humans, this important zoonotic foodborne pathogen encounters various stresses, such as non-growth temperatures, starvation, hypo- and hyper-osmotic stress, and desiccation [5, 6].

Despite the well-known fact that Campylobacter is a fastidious bacterium, human campylobacteriosis cases have significantly increased presumably due to the ability of this pathogen to survive under harsh environmental conditions [7–10] in addition to its low infectious dose (400~800 bacteria) [11]. For example, high genetic diversity of Campylobacter spp. and the ability to transform into a viable-but-non-culturable BIBF 1120 chemical structure state may enhance its adaptability to unfavorable growth conditions [7, 8]. Additionally, biofilm formation and stringent response also contribute to the survival of Campylobacter under Selleck VX-680 stress conditions [9, 10]. However, the molecular mechanisms for stress resistance are still largely unknown in Campylobacter. In many bacterial species, alternative sigma factors play an important role in regulation of stress-defense genes

under hostile environmental conditions [12]. Because a sigma factor can TGF beta inhibitor coordinate gene transcription in response to environmental stimuli, many bacteria possess multiple alternative sigma factors, some of which are often dedicated to stress responses. For example, RpoS is a sigma factor important for adaptive responses in many Gram-negative pathogens, and RpoS mutations in Escherichia coli, Salmonella, Pseudomonas and Vibrio significantly impair bacterial ability to resist various stresses, such as starvation,

low pH, oxidative stress, hyperosmolarity, heat and cold [13–17]. In E. coli, RpoS is involved in resistance to high osmolarity in stationary-phase cells and survival in cold-shock by Aldehyde dehydrogenase regulating one set of RpoS-dependent genes, including otsA and otsB, which are necessary for synthesis of internal trehalose as an osmoprotectant and important for survival at low temperature [18, 19]. In addition, RpoS controls the acid resistance in E. coli by modulating gadC, a gene involved in the glutamate-dependent low pH-resistance, hdeAB, encoding pH-regulated periplasmic chaperons, and cfa, a gene for cycloporpane fatty acid synthesis [20]. As another stress-response sigma factor, RpoE regulates extracytoplasmic functions related to sensing and responding to bacterial periplasmic and extracellular environmental changes, which contributes to heat- and oxidative stress resistance in many Gram-negative bacteria, including E. coli, Pseudomonas and Salmonella [21, 22]. The RpoE mutation in Salmonella reduces bacterial survival and growth in macrophages by the loss of RpoE-dependent gene expression such as htrA, a gene required for oxidative stress resistance [23, 24].

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