Conversely, other genes that inhibit cell cycle progression are down-regulated. These include SKP2, the F-box receptor that interacts with p19 and the CDK2/cyclin A to prevent entry into G1 [36] and SFN (stratifin or 14-3-3σ) a key target of the tumour suppressor gene TP53 which acts to cause G2 arrest [37]. Five other

changes of potential functional importance are of note. Firstly, a number of potentially antibacterial agents are highly induced, including LCN2 (lipocalin-2) [38, 39] and PI3 (peptidase inhibitor 3, aka ELAFIN) [40], whilst MMP7 is thought to activate defensins [41]. Secondly, five key molecules involved in antigen processing and presentation (Figure check details 1, 2) [42] were also up-regulated and could play a role in the development of immune responses to C. jejuni. Thirdly, alterations in matrix metalloproteinases and leukocyte receptors would Selleckchem Ralimetinib influence the inflammatory response,

with MMP9 acting to facilitate neutrophil transfer by activating interleukin-8 [43] and MMP7 acting to localize them to sites of tissue damage [44]. Fourthly, the ephrin pathway (Figure 2), including Ephrin A2 and B2 receptors (EPHA2, EPHB2) and Ephrin A1 (EFNA1, Figure 3), rho kinase (ROCK2), Rac, ARP2/3, CDC42 and WASP appeared to be strongly up-regulated. This pathway is concerned with activation of cytokinetic changes that may potentially play a role in rapid restitution [45, 46]. Finally, up-regulation of the folate receptor (FOLR1) may reflect preparation for reparative nucleotide synthesis dependent upon one-carbon transfer activity [47]. Conclusion The data we have generated using a BCE of C. jejuni

represents a reductionist approach to determine some of the cellular responses associated with C. jejuni infection. However, because C. jejuni Etomidate BCE represents a robust NF-κB inducing activity that is not only heat-stable but resistant to protease and acidic pH (pH 3) [8], these may indeed be of clinical significance if these products are shed upon C. jejuni A-1210477 chemical structure infection or co-delivered through the diet. C. jejuni has been detected in many commercially available chicken portions [2] and clinical cases of Campylobacter enterocolitis are frequently associated with ingestion of partially cooked poultry meat [48]. Changes in host gene expression following C. jejuni BCE interestingly reflects some of the changes that are known to occur in inflammatory bowel diseases (IBD) such as ulcerative colitis, for which C. jejuni colitis can be considered a model, and may therefore indicate other potential targets for investigation of epithelial-derived mediators of inflammation in ulcerative colitis/IBD.