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they have no competing interests. Authors’ contributions Tingsong Hu, Ying Zheng and Yan Zhang participated in the www.selleckchem.com/products/lxh254.html design and conducted the majority of the experiments in the study and drafted the manuscript. Gangshan Li, Wei Qiu and Jing Yu carried out the molecular Lonafarnib clinical trial genetic studies, participated in the sequence alignment. Qinghua Cui,Yiyin Wang, Caoxiong Zhang and Xiaofang Zhou contributed to the interpretation of the findings and revised the manuscript. Ziliang

Feng and Weiguo Zhou performed the analyses of transmission electron microscope. Quanshui Fan and Fuqiang Zhang participated in the design of the study and performed the statistical analysis. All authors read and approved the final manuscript.”
“Background Listeria monocytogenes, a facultative intracellular pathogen, is one of the major causes of food-borne infection in humans [1]. Although rare, invasive listeriosis is a public health concern due mainly to its high fatality rate evaluated at 20-30% [2]. The clinical outcome of listeriosis is influenced by the pathogenic potential of the infecting strain which is in part related to its serotype [3]. It is now known that isolates 1/2a, 1/2b and 4b are responsible for 96% of human infections and most outbreaks are caused by strains of serotype 4b whereas serotype 1/2a has been associated with sporadic cases [4]. Serotypes 4a and 4c are predominant in animal, food or environment [5]. Unfortunately, there is currently no standard definition of virulence levels and no comprehensive overview of the evolution of L. monocytogenes strains taking into account the presence of low-virulence strains [5]. Different studies have shown that L.

Genes were filtered for threshold signal intensities of at least 50 in one biological replicate. Analysis of Variance (ANOVA) was performed to identify statistically significant differences among the three conditions. 910 genes were identified (p-value < 0.01). The gene list was further trimmed to identify genes with fold-change differences of at least 1.5 in any comparison, resulting in 575 LY3039478 molecular weight genes. The log2 values were imported into Genesis [72] for visualization and hierarchical clustering. Data were submitted to Gene Expression Omnibus (NCBI) under accession GSE24118. Subsequent functional enrichment analysis was conducted using the database for annotation, visualization

and integrated discovery (DAVID) software [73]. The functional annotation clustering tool was used to identify over-represented gene ontology terms (p < 0.05; Benjamini correction for multiple testing) with the conservative high stringency option. Significantly upregulated

or downregulated genes with a fold change ± 1.5 (BCM relative to PCM) were submitted as separate lists. Functional annotation clusters with an enrichment score greater than 1.5 were considered significant. Cytokine Detection by ELISA Confluent Vadimezan in vitro HaCaT keratinocytes in 6-well plates were cultured in the presence of bacterial conditioned medium (BCM or PCM) for 4 or 24 hours. Cell culture supernatants were collected and analyzed by colorimetric sandwich enzyme-linked immunoassays (ELISA) for IL-1β, IL-6, TNF-α, CXCL-8, CXCL-1, and GM-CSF (R&D Systems, Minneapolis, MN) following the manufacturer’s instructions. Cytokines in the supernatant were detected as pg/ml. HKs remaining in the culture wells were stained with propidium iodide and counted. Cell counts per well

and the measured percentage of pro-apoptotic cells revealed by Terminal Deoxynucleotidyl Transferase dUTP Nick End Labeling (TUNEL) were used to normalize ELISA data to pg/100,000 adherent, non-apoptotic cells. Detection of MAPK Phosphorylation HaCaT keratinocytes were grown to confluence in clear bottom black walled 96-well plates. Keratinocytes were treated with BCM or PCM for 4 or 24 hours. Total and phosphorylated MAPKs (JNK, p38, and ERK) were why detected simultaneously using a cell-based ELISA (R&D Systems, Minneapolis, MN) following the manufacturer’s instructions. Inhibition of MAPK The p38 MAPK PF-4708671 price inhibitor, SB203580; the ERK inhibitor, U0126; and the JNK inhibitor, SP600125 were prepared as 10 mM DMSO stocks (Cayman Chemicals, Ann Arbor, MI). Confluent HaCaT keratinocytes were pretreated with individual inhibitors or a combination of all three inhibitors (10 μM each, 0.1% DMSO) in EPI growth medium for one hour. Cells were then treated with PCM or BCM supplemented with 10 μM inhibitor(s) for four hours. Cell culture supernatants were collected and analyzed by ELISA for cytokine production. HaCaT keratinocytes treated with PCM or BCM supplemented with 0.1% DMSO were prepared as vehicle controls.

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Leach S, Wilde SJ, Davies A, Stewart GS, Humphrey T: Invasiveness in chickens, Everolimus order stress resistance and RpoS status of wild-type Salmonella enterica subsp. enterica serovar typhimurium definitive type 104 and serovar enteritidis phage type 4 strains. Microbiology 2000,146(Pt 12):3227–3235.PubMed 44. Doyle M, Fookes M, Ivens A, Mangan MW, Wain J, Dorman CJ: An H-NS-like stealth protein aids horizontal DNA transmission in bacteria. Science 2007,315(5809):251–252.CrossRefPubMed 45. Williamson HS, Free A: A truncated H-NS-like protein from enteropathogenic Escherichia coli acts as an H-NS antagonist. Mol Microbiol 2005,55(3):808–827.CrossRefPubMed 46. Navarre WW, Selleckchem SC79 Porwollik S, Wang Y, McClelland M, Rosen H, Libby SJ, Fang FC: Selective silencing of foreign DNA with low GC content by the H-NS protein in Salmonella. Science 2006,313(5784):236–238.CrossRefPubMed 47. Kingsley RA, Humphries AD, Weening EH, De Zoete MR, Winter S, Papaconstantinopoulou A, Dougan G, Baumler AJ: Molecular and phenotypic analysis of the

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48. Herrero A, Rodicio MR, Gonzalez-Hevia MA, Mendoza MC: Molecular epidemiology of emergent multidrug-resistant Salmonella enterica serotype Typhimurium strains carrying the virulence resistance plasmid pUO-StVR2. J Antimicrob Chemother 2006,57(1):39–45.CrossRefPubMed 49. Hradecka H, Karasova D, Rychlik I: Characterization of Salmonella enterica serovar Typhimurium conjugative plasmids transferring resistance to antibiotics and their interaction with the virulence plasmid. J Antimicrob Chemother 2008,62(5):938–941.CrossRefPubMed 50. Gantois I, Ducatelle R, Pasmans F, Haesebrouck F, Van Immerseel F: Salmonella enterica serovar Enteritidis genes induced during oviduct colonization and egg contamination in laying hens. Appl Environ Microbiol 2008,74(21):6616–6622.CrossRefPubMed 51. Clavijo RI, Loui C, Andersen GL, Riley LW, Lu S: Identification of genes associated with survival of Salmonella enterica serovar Enteritidis in chicken egg albumen. Appl Environ Microbiol 2006,72(2):1055–1064.CrossRefPubMed 52. Allen-Vercoe E, Dibb-Fuller M, Thorns CJ, Woodward MJ: SEF17 fimbriae are essential for the convoluted colonial morphology of Salmonella enteritidis. FEMS Microbiol Lett 1997,153(1):33–42.CrossRefPubMed 53. Kado CI, Liu ST: Rapid procedure for detection and isolation of large and small plasmids. J Bacteriol 1981,145(3):1365–1373.PubMed 54.