The strains of Genetic group 1 and the non-typeable strains expressed a great variety of LPS types and subtypes. All 77 Y. enterocolitica 4/O:3 and 3/O:3 strains included in the LPS analysis expressed homopolymeric subtype

check details A3 O-PS and the five Y. enterocolitica 2/O:9 strains subtype A2 O-PS (Table 3). Three of the ystB negative strains of BT 1A Genetic group 1 belonged to LPS group A2, two to C1 and one to B1c. Table 3 LPS types of 298 Y. enterocolitica BT 1A strains and 84 Y. enterocolitica strains of other biotypes LPS-type Subtype Descriptionc Commentsd Known O-serotypes with similar LPS[56] No. of strains selleck screening library (n=382) A. Homopolymeric O-PS   A1a Short   O:41(27)43, O:41,43 7   A2b Medium   O:10 25   A2 Medium BT 2 strains O:9 5   A3a Long     3   A3 Long BT 3–4 strains O:1, O:2, O:3 77 B. Heteropolymeric O-PS   B1a a, B1b a 2/M/1 B1b strains carry homopolymer O:13,18 8   B1c a, B1d a 2+w/M/1–2 B1d strains carry homopolymer O:25 9   B2a a, B2b a 2/L/1 B2b strains carry homopolymer O:7,8, O:13,7 22   B2c a, B2d a 2+w/L/1–2 B2d strains carry homopolymer

O:50 55   B3 a 5–6+w/M/3–6   O:14, O:34, O:4,32 4   B4 a >5/M/7–10   O:4, O:8, O:21, O:35,52 1 C. Single length O-PS   C1 a, SL 15-mer   O:6, O:6,30, O:6,31 109   C2 a SL 30-mer   O:5, O:5,27 45 D. Rough or semi-rough   D a   May include rough laboratory mutants O:15, O:28,50, O:35,36 12 a Biotype 1A, Genetic group 1. b Biotype 1A, Genetic group 2. c Homopolymeric O-PS length

estimated by migration in DOC-PAGE; heteropolymeric O-PS is described by X/Y/Z, where X = number of steps in O-PS ladder (+ w indicates a faint extra step); Y = size of step (M, medium; L, long); Z = average modality of steps; Single length O-PS migrates as one band with estimated number of sugar residues. d The biotype of the strains is 1A unless otherwise indicated. The presence of homopolymeric O-PS was visible as a smear above the short ladders and not always easy to distinguish in silver-stained DOC-PAGE gels. ZD1839 in vitro Phage sensitivity of the strains was tested using five Yersinia specific bacteriophages (Table 4). Most of the 63 bio/serotype 3–4/O:3 strains were sensitive to ϕYeO3-12, PY100 and ϕR1-RT, in addition 7 strains were sensitive to ϕ80-81. The single bio/serotype 2/O:9 strain was infected by ϕR1-RT only. The 273 BT 1A and non-biotypeable strains representing different LPS-types showed variable phage sensitivity patterns further demonstrating the heterogeneity of this group of strains. However, all 17 of the BT 1A Genetic subgroup 2 strains were resistant to all the tested phages. Table 4 Phage sensitivities of 273 Y. enterocolitica BT 1A strains and 64 Y.

These data demonstrate that RCC cells preferentially interact with osteoblasts and extracellular matrix components of the human bone marrow and show increased migration ability in response

to osteoblast-derived factors suggesting a possible mechanism for facilitated homing of RCC cells into bone. Poster No. 110 Tumor-Lymphatic Cross Talk Contributes to Tumor Progression and Invasion Jacqueline D. Shields 1 , Amine Issa1, Iraklis C. Kourtis1, Melody A. Swartz1 1 Institute for Bioengineering, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland Changes in the immunological equilibrium and escape from immune surveillance are critical events for the progression of a developing Linsitinib concentration tumor. Likewise, tumor derived vascular endothelial

growth factor C (VEGF-C) is known to stimulate lymphatics at the tumor periphery and promote metastasis to draining lymph nodes. CCL19 and CCL21 are produced by both lymphatic endothelium and reticular stroma guiding antigen presenting cells (APCs) to LN and driving co-localization of CCR7+ APCs and naïve T cells within selleck kinase inhibitor the lymph node. Furthermore, we recently demonstrated that tumors use autologous CCL21 secretion and lymphatic function to escape a growing tumor. To this end, we investigated how lymphatic growth factors and lymph node chemokines influence the developing tumor-lymphatic microenvironment and ensuing immune response. We engineered tumor cells

to secrete different levels of CCL21 and VEGF-C. Using in vitro co-culture models and complementary in vivo studies we demonstrate that several tumor cell lines express functional VEGFR-3; hence tumor-derived VEGF-C could act autologously on tumor cells to promote their invasion through a 3D matrix, by increasing their motility and proteolytic activity. In addition to peritumoral lymphatic expansion, Sclareol tumor-secreted VEGF-C also increased CCL21 production by lymphatic endothelium. Increased tumor volumes were observed in these VEGF-C-overexpressing tumors compared with control counterparts and coincided with a switch in the inflammatory compartment towards a regulatory phenotype. A sustained loss of CCL21 at the tumor site permitted an effective tumor specific immune response to develop. These results indicate that modulation of the tumor-lymphatic microenvironment not only promotes metastasis through VEGF-C-CCL21 cross-talk strategies but is also necessary for manipulation and control of the anti-tumor immune response. Poster No.

In this study, we focused on 2D solid silica sphere film made by LB technique and its superior antireflection effect. A parametric study of deposition conditions is conducted and correlated to the resulting film

morphology and optical properties. We demonstrated that the thin films of single-layer solid silica nanospheres with a diameter of approximately selleck compound 100 nm could offer comparable AR effect with respect to the mesoporous counterparts. Furthermore, the transmission peak of the nanosphere silica AR coating can be controlled by varying the LB deposition parameters. To our best knowledge, no such peak-tunable property has been reported before, although spectral shift due to the thickness of mesoporous Fluorouracil purchase silica spheres’ thin film has been observed in previous works [4, 5, 9, 10]. The deposition parameters which determine the peak transmission wavelength are extracted.

Three variables, namely deposition pressure, surfactant concentration and solution ageing, were found to strongly correlate with the maximum transmission position. Film density and aggregations of nanospheres resulting from the above variables are considered as principal determining factor behind this shift. The ability of achieving broadband transmission and simultaneously being able to determine the position of maximum transmission (>99%) opens the possibility of many application-specific solutions. For photovoltaics, for instance, it is possible to match the absorption peak of absorber materials by tuning the transmission peak of glass. For displays, it can reduce reflection and glare, while transmitting more of the display light, thereby requiring lower intensity light and reducing energy consumption. Methods ALOX15 All chemicals were used as received, without any further purification. Aqueous suspension of silica spheres (50 mg/ml, polydispersity index <0.2, diameter 100 nm) were purchased from Kisker

Biotech GmbH & Co, Steinfurt, Germany. The silica sphere suspension was diluted down to 10 mg/ml with pure ethanol (ACS reagent, ≥99.5%, absolute, Sigma-Aldrich, St. Louis, MO, USA) and then mixed with hexadecyltrimethylammonium bromide (CTAB; ≥98%, Sigma-Aldrich). CTAB was used to change the hydrophilic/hydrophobic nature of the silica spheres. The final diluted suspension with CTAB was ultrasonicated for 30 min each time before deposition. Microscope glass slides (Agar Scientific, Essex, UK, 76 mm × 26 mm) were cleaned in acetone, IPA and DI water subsequently in an ultrasonic bath for 10 min at each step. After cleaning, glass slides were treated with oxygen plasma (Philips RIE, New York, USA). Both sides of the slides were treated by 100-W O 2 plasma for 5 min at a pressure of 150 mbar. Monolayer of silica nanospheres were deposited onto plain glass slides using a Langmuir-Blodgett trough (NIMA Technology model 612D, Coventry, UK). The deposition process and mechanism has been discussed by many previous reports [17–19].

However, the cell membrane is likely to have undergone some degree of lipolysis as a result of an imbalance in calcium homeostasis [4], almost certainly from GSK-3 inhibitor the exercise insult. The damage

literature often shows a high degree of inter-subject variability in CK and other cytosolic markers of EIMD, however, variability in the current study was relatively small, partly attributable to the trained status of the volunteers. The greater conditioning of these participants has almost certainly led to a repeated bout effect [31], whereby, a conditioning bout of exercise (in this case prior training) leads to a decrease in damage indices on subsequent bouts [4, 31, 32]. This is further learn more supported by the low CK response seen in both groups following the exercise, when compared to the damage responses seen in untrained volunteers [19, 20]. Despite this relative homogeneity, the CK response was less in the BCAA group suggesting the membrane integrity was maintained to greater extent than the placebo group. The damage response is known to be bi-phasic in nature; a primary response caused

by the mechanical stress of the exercise, followed by a secondary, transient inflammatory response over the following hours and days [4]. The subsequent inflammatory response increases protein uptake necessary for use as an energy source and/or pathways responsible for cell signaling and subsequent muscle remodeling [14, 33]. Although we cannot definitively support this postulate, it seems plausible that the greater bioavailability provided by BCAA facilitated

this response and thereby decreased secondary damage to the muscle. Our data concur with previous studies that show a peak in soreness at 48 h post-exercise [27, 32]. Furthermore, the group effects support ID-8 previous data [20, 21, 34] showing a reduction in muscle soreness following a damaging bout of exercise with BCAA supplementation. Although the mechanism surrounding muscle soreness following a damaging bout of exercise is not well understood, it seems likely to be related to inflammation, particularly to the connective tissue elements [35] that sensitise nociceptors in muscle and hence increase sensations of pain [36]. However, previous work [20] demonstrating a reduction in soreness following BCAA supplementation also measured the acute inflammatory response (interleukin-6, a pro-inflammatory cytokine) and showed no difference between the BCAA and placebo groups. Jackman et al. [20] suggested that the increase in food or feeding per se, particularly amino acids, might be related to reductions in soreness. Although this idea is somewhat speculative and has no supporting evidence or proposed mechanism, we show similar trends in our data, but it is not possible to support or refute this theory.

Science 1998, 282:1494–1497.CrossRefPubMed 5. Mulvey MA, Schilling JD, Hultgren

SJ: Establishment of a persistent Escherichia coli reservoir during the acute phase of a bladder infection. Infect Immun 2001, 69:4572–4579.CrossRefPubMed 6. Anderson GG, Palermo JJ, Schilling JD, Roth R, Heuser J, Hultgren SJ: Intracellular bacterial biofilm-like pods in urinary tract infections. Science 2003, 301:105–107.CrossRefPubMed 7. Johnson JR: Microbial virulence determinants and the pathogenesis of urinary tract infection. Selleckchem CT99021 Infect Dis Clin North Am 2003, 17:261–78. viii.CrossRefPubMed 8. Taylor PW: Bactericidal and bacteriolytic activity of serum against gram-negative bacteria. Microbiol Rev 1983, 47:46–83.PubMed 9. Martinez JJ, Mulvey MA, Schilling JD, Pinkner JS, Hultgren SJ: Type 1 pilus-mediated bacterial invasion of bladder epithelial cells. EMBO J 2000,

19:2803–2812.CrossRefPubMed 10. Selvarangan R, Goluszko P, Popov V, Singhal J, Pham T, Lublin DM, Nowicki S, Nowicki B: Role of decay-accelerating factor domains and anchorage in internalization of Dr-fimbriated Escherichia coli. Infect Immun 2000, 68:1391–1399.CrossRefPubMed 11. Doye A, Mettouchi A, Bossis G, Clement R, Buisson-Touati C, Flatau G, Gagnoux L, Piechaczyk M, Boquet P, Lemichez E: CNF1 exploits the ubiquitin-proteasome machinery to restrict Rho GTPase activation for bacterial host cell invasion. Cell 2002, 111:553–564.CrossRefPubMed www.selleckchem.com/products/ABT-737.html 12. Springall T, Sheerin NS, Abe K, Holers VM, Wan H, Sacks SH: Epithelial secretion all of C3 promotes colonization of the upper urinary tract by Escherichia coli. Nat Med 2001, 7:801–806.CrossRefPubMed

13. Li K, Feito MJ, Sacks SH, Sheerin NS: CD46 (membrane cofactor protein) acts as a human epithelial cell receptor for internalization of opsonized uropathogenic Escherichia coli. J Immunol 2006, 177:2543–2551.PubMed 14. Li K, Sacks SH, Sheerin NS: The classical complement pathway plays a critical role in the opsonisation of uropathogenic Escherichia coli. Mol Immunol 2008, 45:954–962.CrossRefPubMed 15. O’Hanley P, Lark D, Falkow S, Schoolnik G: Molecular basis of Escherichia coli colonization of the upper urinary tract in BALB/c mice. Gal-Gal pili immunization prevents Escherichia coli pyelonephritis in the BALB/c mouse model of human pyelonephritis. J Clin Invest 1985, 75:347–360.CrossRefPubMed 16. Racusen LC, Monteil C, Sgrignoli A, Lucskay M, Marouillat S, Rhim JG, Morin JP: Cell lines with extended in vitro growth potential from human renal proximal tubule: characterization, response to inducers, and comparison with established cell lines. J Lab Clin Med 1997, 129:318–329.CrossRefPubMed 17. Caprioli A, Falbo V, Roda LG, Ruggeri FM, Zona C: Partial purification and characterization of an escherichia coli toxic factor that induces morphological cell alterations. Infect Immun 1983, 39:1300–1306.PubMed 18.

Therefore, the drug was released incompletely from the NPs in 48 h. Thus, PTX-MPEG-PLA NPs are promising in the expansion of dosing range of chemotherapeutic drugs and rendering patients safe cancer therapy. Additionally, it was interesting to note that the cell viability in PTX-MPEG-PLA NPs was higher than that in PTX-PLA NPs at a series of increasing concentrations (2.5, 10, 20, and 40 μg/mL). This result can most likely be attributed to the drug release rate of the PTX-MPEG-PLA NPs being higher than that of the PTX-PLA NPs. Figure 7 In vitro cell viability assays PI3K inhibitor for growth inhibition effect after 48

h ( n  = 6). Conclusions In our previous study, a simple but successful method was developed to obtain PTX-MPEG-PLA NPs with appropriate formulation characteristics including small particle size, narrow particle size distribution,

high zeta potential, satisfactory drug encapsulation efficiency, and appreciable drug-loaded content. The PTX-MPEG-PLA NPs presented a faster drug release rate but minor burst release as well as a higher cell cytotoxicity learn more compared to the PTX-loaded PLA NPs. A further study on the in vivo pharmacokinetics and antitumor effects of PTX-MPEG-PLA NPs is currently in progress. Acknowledgements This work was funded by the National Natural Science Foundation of China (grant nos. 81000660 and 31271071) and Xiamen Science and Technology Project (3502Z20123001 and 3502Z20114007). References 1. Peer D, Karp JM, Hong S, Farokhzad OC, Margalit R, Langer R: Nanocarriers as an emerging platform for cancer therapy. Nat Nanotechnol 2007, 2:751–760.CrossRef 2. Petros RA, DeSimone JM: Strategies in the design of nanoparticles for therapeutic applications. Nat Rev Drug Discovery 2010, 9:615–627.CrossRef 3. Adair JH, Parette MP, Altinoglu EI, Kester M: Nanoparticulate Rho alternatives for drug delivery. ACS Nano 2010, 4:4967–4970.CrossRef 4. Kievit FM, Zhang M: Cancer nanotheranostics: improving imaging and therapy by targeted delivery

across biological barriers. Adv Mater 2011, 23:H217–247.CrossRef 5. Elsabahy M, Wooley KL: Design of polymeric nanoparticles for biomedical delivery applications. Chem Soc Rev 2012, 41:2545–2561.CrossRef 6. Davis ME, Chen ZG, Shin DM: Nanoparticle therapeutics: an emerging treatment modality for cancer. Nat Rev Drug Discovery 2008, 7:771–782.CrossRef 7. Mai Y, Eisenberg A: Self-assembly of block copolymers. Chem Soc Rev 2012, 41:5969–5985.CrossRef 8. Schacher FH, Rupar PA, Manners I: Functional block copolymers: nanostructured materials with emerging applications. Angew Chem Int Ed 2012, 51:7898–7921.CrossRef 9. Nie Z, Petukhova A, Kumacheva E: Properties and emerging applications of self-assembled structures made from inorganic nanoparticles. Nat Nanotechnol 2010, 5:15–25.CrossRef 10. Kwon GS, Kataoka K: Block copolymer micelles as long-circulating drug vehicles. Adv Drug Delivery Rev 2012, 64:237–245.CrossRef 11. Rowinsky EK, Donehower RC: Paclitaxel (taxol).

Replicates within experiments are expressed as a mean for a single experiment. ANOVA and unpaired Student’s t-test were conducted using InStat3 (GraphPad, San Diego, CA). Means were compared using ANOVA and Tukey’s post-hoc test. Results AIEC infection decreases TER in T84 and MDCK-I epithelial cell monolayers Similar to EHEC O157:H7, apical infection for 16 h with AIEC, strain

LF82 caused a 46% reduction in TER in human colonic T84 cells (Figure 1A; ANOVA: p < 0.01, compared with uninfected sham controls). When the pathogen was introduced into the basolateral aspect of monolayers there was an 81% reduction in TER, relative to sham control monolayers, with AIEC infection (p < 0.001), compared to a 50% reduction with EHEC BEZ235 in vivo infection (p < 0.01; t test of AIEC vs. EHEC: p = 0.052). In contrast, both apical and basolateral infection of T84 monolayers with non-pathogenic E. coli, strain HB101 did not lead to a reduction in TER (N = 2). Figure 1 AIEC, strain LF82 disrupts the integrity of polarized selleck inhibitor epithelial monolayers. Model epithelial cell monolayers [T84 (Panel A) and MDCK-I

(Panels B & C)] grown in Transwells were infected with either E. coli, strain LF82 (AIEC) or EHEC O157:H7 – employed as a positive control – for 16 h at 37°C. Both apical (black bar histograms) and basolateral (gray bars) infections of human intestinal T84 monolayers caused a reduction in TER (Panel A; N = 4–6). Similar effects of infection on monolayer integrity were observed when MDCK-I cell monolayers were infected with AIEC, strain LF82 (Panel B), together with an increase in permeability to a macromolecular (10-kilodalton) dextran probe, indicating barrier disruption (Panels C; N = 2–4). HK denotes heat-killed bacteria. ANOVA: * p < 0.05; ** p < 0.01; *** p < 0.001. Apical and basolateral infections of canine kidney-derived MDCK-I polarized monolayers with EHEC and AIEC caused a comparable reduction of 53–73% in TER (Figure 1B; ANOVA: p < 0.01). Live bacteria were required, because there was no drop in TER with either heat-inactivated

or formaldehyde-fixed Rho bacteria (Figure 1B). The effects were not due to the metabolic activity of bacteria on epithelial cells, since incubation with tissue culture medium corrected to pH 6 (the pH of medium after 16 h of infection) did not reduce TER (N = 2). Macromolecular permeability increases following AIEC infection of MDCK-I monolayers Transcytosis of a 10-kDa dextran probe across monolayers supported the TER results. Consistent with previous reports [26], EHEC O157:H7 caused a dramatic increase in permeability to dextran, indicating breakdown of the epithelial barrier. Infection with AIEC also resulted in increased dextran permeability in MDCK-I cells (ANOVA: p < 0.05 for basolateral AIEC infection) comparable to findings seen with EHEC infection (Figure 1C; p > 0.05). There was a similar, but more modest, increase in permeability of T84 monolayers infected with AIEC (data not shown).

e., non-traumatic, phakic) RRD. Although in Italy the age ranges for the working population are wider (at the 2001 census about find more 62,000 workers were aged 75 years or older), for the calculation of rates among Tuscan manual and non-manual workers and housewives, we restricted the study population to subjects aged 25–59 years because of limited numbers of cases in the youngest age groups and large numbers of retired subjects in the oldest age groups. We also excluded

members of the armed forces (due to the difficulty in determining whether their work was manual or non-manual); students (due to possible misclassification in the case of students with concurrent occupational exposure); cases with undeclared/unknown

employment status (due to treatment outside Tuscany); unemployed or retired subjects (due to lack of information about previous occupational status); people yet to obtain a first job; and patients with “other” (unspecified) job titles. No house husbands were reported among surgically treated cases of RRD in Tuscany. To obtain population data for the age groups of interest in the study area, including numbers of manual workers, non-manual workers and full-time housewives, we referred to the closest national census, conducted in 2001 by the National Institute of Statistics (ISTAT). Statistical analysis We calculated age- and sex-specific incidence rates (per 100,000 person-years) for manual workers, non-manual workers and housewives, and also overall rates directly standardized according to the Standard European Population proposed by the World Health Organization (Waterhouse Opaganib et al. 1976). We calculated age-specific rate ratios (RRs) for male and female manual workers and housewives, taking non-manual workers as the reference category. The likelihood ratio statistic was used to test the null hypothesis that the two rates of

interest were equal (Kirkwood and Sterne 2003). To test trends in incidence rates across five-year age bands, we used the score test and derived RR estimates for a unit increase in age class (Clayton and Hills 1993). For both rates and RRs, we calculated 95 % CI. Since the hospital discharge records database selleck compound did not permit identification of patients in years before the observation period, we carried out a sensitivity analysis in which we excluded the first 2 years of the observation period (i.e., 1997 and 1998) to explore the possibility that the main analysis might have been distorted by the inclusion of some readmissions of prevalent cases. Stata 11.2 SE (Stata Corporation, Texas, TX, USA) was used for analysis with a significance level of 0.05. Results Data on employment were available for 2,444 (89 %) of 2,753 surgically treated cases of idiopathic RRD among Tuscan residents aged 25–59 years (age exclusions: ≥60 years, n = 4,120; <25 years, n = 178).

Controls could be composed of healthy subjects, chronic liver disease (CLD), including chronic hepatitis (CH) and LC. CLD was either histologically proven or diagnosed based on concordant clinical, biological, and morphological criteria. Review articles and articles that did not provide genotype data were excluded. Data extraction and synthesis this website The following information was extracted from each study: first

author’s surname, year of publication, ethnicity of study population, country where study was conducted, and the number of cases and controls for each C282Y and H63D genotype. When specific results were not reported, we used available tabular data to calculate them. Statistical methods To compare the odds ratio (OR) on the same baseline, we used crude OR to conduct the meta-analysis. The effect of association was indicated as crude OR with the corresponding 95% confidence intervals (CIs). Because of relatively small sample sizes of individual studies and low frequency of variant alleles and the practical clinical value, we performed meta-analysis only in two models: dominant www.selleckchem.com/products/R788(Fostamatinib-disodium).html model (YY+CY vs. CC or DD+HD vs. HH) and

allele contrast (Y vs. C or D vs. H). The pooled OR was estimated using the FE model (DerSimonian & Laird) [22]. The heterogeneity between ifenprodil studies was tested using the Q statistic [23]. If P < 0.10, the heterogeneity was considered

statistically significant, and the RE model was then used. Heterogeneity was also quantified using the I2 metric, which is independent of the number of studies in the meta-analysis (I2 < 25% = no heterogeneity; I2 = 25-50% = moderate heterogeneity; I2 > 50% = large or extreme heterogeneity) [24]. The potential small-study bias was tested using the Egger regression test asymmetry [25] and the Begg’s test for funnel plot, which is based on Kendall’s tau [26]. Sensitivity analysis was performed by omitting one study at a time to assess the influence of individual studies on meta-analysis. The distribution of the genotypes in the control group was tested for Hardy-Weinberg equilibrium using a goodness-of-fit Chi-square test. All analyses above were conducted using the STATA version 10.0 software (Stata Corp, College Station, Texas). All P-values were two-sided. A p value less than 0.05 was considered statistically significant. The statistical power was calculated using the PS software [27]. In order to assess the reliability of the positive association, we calculated false positive report probability (FPRP) [28]. An Excel spreadsheet to calculate FPRP is included with the online material http://​jncicancerspectr​um.​oupjournals.​org/​jnci/​content/​vol96/​issue6. If FPRP < 0.

If free Fe2+

is present in the cell, the produced H2O2 can form hydroxyl radicals (·OH), which may directly damage DNA. This may explain the induced production of Dps that reversibly binds iron. The produced H2O2 can be removed by catalase (KatA) which converts H2O2 to H2O and O2[37, 57]. In contrast to a transcriptional study where an up-regulation of katA gene was noticed after acid exposure [24], induction of KatA was not observed in this proteomic study. Since C. jejuni is sensitive towards oxygen and lacks numerous oxidative stress regulators such as SoxRS and OxyR [13], the cell might be in a constantly oxygen-alert state in order to remove reactive oxygen species and damaging components from acid stress. No induction of heat Ferroptosis activation shock proteins (Hsps) as chaperones or proteases were observed during acid stress in this study. A transcriptional study found an up-regulation of clpB, dnaK, grpE, groEL/ES and htrA[24]. One explanation could be the sensitivity of 2D-gel-electrophoresis for proteomic analysis as mentioned selleckchem above and the detection limit due to molecular size and isoelectric point (pI) of the proteins. The Hsps, ClpP and GroES have molecular masses

close to the maximum and minimum detection size, respectively, and HtrA has a pI of 9.6 which is outside the pI range of the system used here. Acid exposure of C. jejuni NCTC 11168 was related to changes in gene expression and synthesis of acid stress proteins. However, comparison of the proteomic and transcription study showed a limited correlation between induced proteins and over-expression of genes. A recent proteomic study with acid adaptation of Salmonella enterica also [26] found a limited correlation between the outcomes of the transcriptional (qRT-PCR) versus translational (2D-gel) studies. The lack of corresponding

results may be due to the lifetime of the RNA and Molecular motor the time from transcription to translation. Conclusions It can be concluded that the three C. jejuni strains, at the phenotypic and proteomic level, responded differently to the acid stresses. We demonstrated that acid stress induces production of several proteins normally involved in iron control and oxidative stress defence in C. jejuni. This work has contributed to the understanding of what occurs in the C. jejuni cells during acid stress. Acknowledgements This work was financially supported by the Danish Food Industry Agency. We acknowledge Bjarne Albrektsen for excellent technical assistance during development and optimization of the chemically defined broth; Andrea Maria Lorentzen from the University of Southern Denmark, who has been a great help in identifying proteins; and Søs Inger Nielsen for excellent technical assistance with qRT-PCR runs. Dr. Thomas Alter, Freie Universitet Berlin, generously provided the strains 305 and 327. References 1. Birk T, Knøchel S: Fate of food-associated bacteria in pork as affected by marinade, temperature, and ultrasound.