Cultures were inoculated with approximately 104 CFU/mL of each strain and incubated under normal conditions. At 6 h, SE1457ΔsaeRS and SE1457 had log CFU/mL counts of 8.2 of and 8.4, respectively. CFU counts were also similar at 12 h post-inoculation, with log CFU/mL counts of 8.1 and 8.6 for SE1457ΔsaeRS and SE1457 respectively. Selleck INCB024360 However, after 24 h, SE1457ΔsaeRS cultures had a lower CFU count (8.3 log CFU/mL) compared to the wild-type strain (9.7 log CFU/mL) (P = 0.002) (Figure 5A). Figure 5 Viability of S. epidermidis 1457 in biofilms

and the planktonic state. (A) CFU counts of SE1457ΔsaeRS and SE1457. After 0, 6, 12, and 24 h of incubation, CFUs for SE1457 and SE1457ΔsaeRS cultures were calculated using serial dilutions of each sample plated on 6 agar plates. (B) CLSM images of S. epidermidis biofilms. IWR-1 mw SE1457 and SE1457ΔsaeRS were incubated in glass-bottomed cell culture

dishes. After incubation at 37°C for 24 h, SE1457ΔsaeRS and SE1457 cells in biofilms were stained with LIVE/DEAD reagents that indicate viable cells by green fluorescence (SYTO9) and dead cells by red fluorescence (PI). Results depict a stack of images taken at approximately 0.3 μm depth increments and represent one of the three experiments. Fluorescence intensities were quantified using ImageJ software. WT, SE1457; SAE, SE1457ΔsaeRS. The viability of SE1457ΔsaeRS and the wild-type strain in 24 h biofilm was determined by confocal laser buy GDC-0973 scanning microscopy (CLSM) with LIVE/DEAD staining [34]. More dead cells were observed in the SE1457ΔsaeRS biofilm compared to the wild-type strain (Figure 5B). Effect of saeRS deletion on eDNA release from S. epidermidis Extracellular DNA is an important component of the S. epidermidis biofilm matrix [7, 35], and its relative concentration in 24 h biofilms formed by SE1457,

SE1457ΔsaeRS and SE1457saec was measured utilizing qPCR for gyrA, lysA, serp0306, and leuA [19, 28]. Extracellular DNA concentrations were increased in the SE1457ΔsaeRS biofilms compared to the complementation strain and the wild-type strain (Figure 6). Figure 6 Quantification of eDNA in SE1457 ΔsaeRS , SE1457, and SE1457 saec filipin biofilms. eDNA was extracted from the unwashed 24 h biofilms of SE1457ΔsaeRS (white bars), SE1457 (black bars), and SE1457saec (gray bars). The eDNA in each biofilm was quantified by qPCR using primers specific for gyrA, serp0306, lysA, and leuA [19, 28]. The quantity of eDNA was calculated as follows: total eDNA (ng)/relative OD600. Results represent the mean ± SD of three independent experiments. WT, SE1457; SAE, SE1457ΔsaeRS; SAEC, SE1457saec. When DNase I (28 U/200 μL/well) was added prior to biofilm formation, the biomass of the SE1457ΔsaeRS biofilms was decreased by 4-fold (P < 0.05); in contrast, the biomasses of SE1457 and SE1457saec biofilms were decreased by 1.5-fold (Figure 1).

A second major reason for conversion from LDR to HDR is reduced hospitalization. For each LDR patient of around one week of hospitalization is required, whereas, with HDR, this can be reduced to a maximum of one day. In many countries, hospitalization of patients is very expensive and methods to check details reduce this cost are encouraged. In others, the availability of hospital beds is a problem, especially beds in rooms suitably placed or shielded for LDR brachytherapy. There is also the problem of morbidity due to the long periods of bed-rest associated with LDR treatments. One concern with LDR

intracavitary Selleckchem Lazertinib brachytherapy is the stability of positioning of the applicators during the long periods of treatment. Dose calculations are performed soon after the applicators are inserted and before they are loaded. On the few occasions that a second dosimetric study has been performed on treatment completion,

this assumption has been shown to be erroneous. For example, a recent study of data from five institutions where dose distributions have been determined both at the VX-809 mw beginning and at the end of an intracavitary application with LDR has demonstrated that ‘hot-spot’ dose rates to bladder and rectum increased during treatment at an average rate of 7% and 19% respectively, with negligible change in the dose rate to Point A [47]. Our results comparing late rectal and bladder complications in patients treated by HDR brachytherapy to LDR brachytherapy show that there is no difference between these two techniques. Similar probability of late complications in rectal, bladder or small intestine was observed in both groups (Table 4). Theoretically, HDR involves a greater probability of late effects for a given level of tumor control; however, the fractionation of HDR intracavitary brachytherapy appears to offset this difference in tumor and normal tissue effects caused by an increase in dose rate. Despite its radiobiological disadvantages mentioned by Eifel [48], the possibility of optimizing dose distribution and the lesser chance of applicator displacement

seem to outweigh these disadvantages. Furthermore, the variation of dwell time with the single stepping source permits an almost infinite variation on the effective source strength and source positions, Casein kinase 1 which allows for greater control of dose distribution and potentially less morbidity [25]. None of the RCTs in the literature show a higher incidence of late complications in patients with cervix cancer treated with HDR brachytherapy compared to those treated with LDR. In our meta-analysis, incidence of lower 5-year rectal complication in patients from the HDR group was probably the result of the relatively low dose delivered to the rectum with the HDR brachytherapy fractionation used. In LDR brachytherapy, the total rectal dose was commonly limited to 70 Gy.

App Environ Microbiol 1997,63(5):2047–2053. 49. Wadowsky RM, Yee RB: Satellite growth of Legionella FRAX597 pneumophila with an environmental

isolate of Flavobacterium breve . App Environ Microbiol 1983,46(6):1447–1449. 50. James BW, Mauchline WS, Fitzgeorge RB, Dennis PJ, Keevil CW: Influence of iron limited continuous culture on physiology and virulence of Legionella pneumophila . Infect Immun 1995,63(11):4224–4230.PubMed 51. Toze S, Sly LI, MacRae IC, Fuerst JA: Inhibition of growth of Legionella species by heterotrophic plate count bacteria isolated from chlorinated drinking water. Curr Microbiol 1990,21(2):139–143.CrossRef 52. Temmerman R, Vervaeren H, Noseda B, Boon N, Verstraete W: Necrotrophic growth of Legionella pneumophila . App Environ Microbiol 2006,72(6):4323–4328.CrossRef 53. Rogers J, Keevil CW: Immunogold

and fluorescein immunolabeling of Legionella pneumophila within an aquatic biofilm visualized JSH-23 cost by using episcopic differential interference contrast microscopy. App Environ Microbiol 1992,58(7):2326–2330. 54. Azevedo NF, Almeida C, Cerqueira L, Dias S, Keevil CW, Vieira MJ: Coccoid form of Helicobacter pylori as a morphological manifestation of cell adaptation to the environment. App Environ check details Microbiol 2007,73(10):3423–3427.CrossRef 55. Azevedo NF, Pinto AR, Reis NM, Vieira MJ, Keevil CW: Shear stress, temperature, and inoculation concentration influence the adhesion of water-stressed Helicobacter pylori to stainless steel 304 and polypropylene. App Environ Microbiol 2006,72(4):2936–2941.CrossRef 56. Mouery K, Rader BA, Gaynor EC, Guillemin K: The stringent response is required for Helicobacter pylori survival of stationary phase, exposure to acid, and aerobic shock.

J Bacteriol 2006,188(15):5494–5500.PubMedCrossRef 57. Nilsson H-O, Blom J, Al-Soud WA, Ljungh A, Andersen LP, Wadstrom T: Effect of cold starvation, acid stress, and nutrients on metabolic activity of Helicobacter pylori . App Environ Microbiol next 2002,68(1):11–19.CrossRef 58. West AP, Millar MR, Tompkins DS: Effect of physical environment on survival of Helicobacter pylori . J Clin Pathol 1992,45(3):228–231.PubMedCrossRef 59. Winiecka-Krusnell J, Wreiber K, Von Euler A, Engstrand L, Linder E: Free-living amoebae promote growth and survival of Helicobacter pylori . Scand J Infect Dis 2002,34(4):253–256.PubMedCrossRef 60. Dailloux M, Laurain C, Weber M, Hartemann P: Water and nontuberculous mycobacteria. Water Res 1999,33(10):2219–2228.CrossRef 61. Fischeder R, Schulzerobbecke R, Weber A: Occurrence of mycobacteria in drinking water samples. Zentralblatt fur Hygiene und Umweltmedizin 1991,192(2):154–158.PubMed 62. Gião M, Wilks S, Azevedo N, Vieira M, Keevil C: Validation of SYTO 9/Propidium Iodide Uptake for Rapid Detection of Viable but Noncultivable Legionella pneumophila. Microb Ecol 2009,58(1):56–62.PubMedCrossRef 63.

The MIRU-VNTR technique provides numerous advantages: it provides a rapid, adaptable technique to comment on selleck products the presence of clonal complexes within isolates linked using an epidemiological method [16]. Coding the results as a series of numbers allows an easy exchange of results between different labs. On the practical side, this

technique also enables evaluation of the possibility of laboratory contamination in cultures from different isolates. Using MIRU-VNTR markers, we also confirmed the identity of isolates collected from the same patients when they had a relapse of their illness. This stability was observed invitro with subcultures of the same isolate, and invivo for the same infected patient. This result contrasted with results obtained by the MIRU-VNTR technique on strains of M. tuberculosis, which provided an example of frequent exogenous infections [17]. We did not find any difference in the genetic profile of serial strains found in our patients, which permitted us to exclude the possibility of re-infection with a new strain of M. intracellulare. For the clustering analysis of MIRU-VNTR profiles, a graphing algorithm termed minimum spanning tree was used. This method has been introduced by some authors to improve LDN-193189 in vitro analysis of VNTR

profiles [14]. Similar to maximum-parsimony phylogenetic tree reconstruction methods, minimum spanning tree constructs a tree that connects all the genetic profiles Venetoclax clinical trial in such a way that the summed genetic distance of all branches is minimized. The differences in mathematical approach between minimum spanning tree and UPGMA methods explain changes in strains clustering. Thus, minimum spanning tree allowed us to group strains which were unclustered with UPGMA (isolates 54 in complex II and 34 in complex I). Our study permitted us to

characterize the statistical power of the MIRU-VNTR technique as AS1842856 cell line applied to M. intracellulare. The global discriminatory index of 0.98 presented in this work confirmed the possible use of this technique, in agreement with results obtained with other species of the avium complex [7]. Interestingly, Ichikawa et al. [10] also described an HGDI of 0.98 for the MLVA of M. intracellulare. Forty-four MIRU-VNTR types were obtained in our study for the 61 M. intracellulare clinical isolates, a number similar to that described by Ichikawa [10]. Our results confirmed the data very recently described for M. intracellulare [10] showing that this method seemed to harbor a great discriminatory power for identification of genetically similar isolates. Mycobacterium avium-intracellulare complex agents, in addition to a broad host range, are environmental mycobacteria found in numerous biotopes including the soil, water, aerosols, and vegetation. Nevertheless, little is known about genetic variations among patient and environmental isolates of M. intracellulare.

We focused on reporting the results of stage A and B patients because most of the patients in advanced BCLC stages (stage C and D) received only palliative care and no active treatment at that time. Furthermore, patients with advanced BCLC stages typically suffer from complications of terminal liver cirrhosis which has a considerable influence on survival. To minimize the influence of the underlying liver disease and to focus on the impact of tumour treatment

on survival, patients with advanced BCLC stages were excluded. MELD scores within the BCLC stages A and B, respectively and various treatment modalities were not statistically significant learn more when tested allowing for multiple comparisons (p = 0.07). The demographic data and clinical characteristics are given in Table 1. Liver cirrhosis was diagnosed either by histology or by the typical combination of laboratory tests, clinical and gastroscopic findings and typical signs of liver cirrhosis in CT or ultrasound. Diagnosis of hepatocellular carcinoma was done according to the criteria of EASL [15] and AASLD [16]. Histologic confirmation was performed in 31 of 40 (77.5%) patients in BCLC stage A and 50 of 55 (90.9%) patients with BCLC stage B. Overall, hepatocellular

carcinoma was histologically confirmed GSK1210151A order in 85.3% of our patients. Table 1 Characteristics of patients with HCC according to treatment modalities the     Sandostatin LAR TACE multimodal therapy palliative care     BCLC A BCLC B BCLC A BCLC B BCLC A BCLC B BCLC A BCLC B number   11 14 5 9 7 10 17 22 Sex                     male 6 10 4 8 7 9 14 16   female 5 4 1 1 0 1 3 6 liver cirrhosis                     no 0 0 0 2 1 0 2 2   yes 11 14 5 7 6 10 15 20 Child-Pugh-classification                     Child A 9 12 1 3 5 8 7 7   Child

B 2 2 4 4 1 2 8 13   Child C 0 0 0 0 0 0 0 0 MELD (median/range)   7.33 (0.27-15.98) 7.61 (0.16-15.0) 14.60 (11.13-17.35) 11.46 (6.68-16.90) 11.56 (6.78-49.26) 8.98 (7.15-16.01) 12.31 (4.66-58.20) 13.20 (1.53-49.82) Etiology                     Alcoholism 5 8 2 4 5 3 8 8   chronic hepatitis B 1 0 0 0 1 0 2 0   chronic hepatitis C 4 4 3 2 1 7 5 7   others 1 2 0 3 0 0 2 6 Age (median/range)   66.5 (53.7-80.5) 68.7 (49.4-73.4) 64.9 (63.6-69.2) 68.4 (48.4-78.4) 50.5 (47.4-64.6) 69.9 (61.2-76.9) 68.5 (43.1-81.2) 62.5 (44.8-73.4) Treatment modalities Long-acting Octreotide [Sandostatin LAR] 30 mg long-acting octreotide (Sandostatin-LAR™, Novartis, Basel, MK-0518 Switzerland) was given i.m. once a month until death. This therapy was given within the context of an unpublished study to compare the clinical outcome of additional percutaneous ethanol instillation (PEI) against no further treatment in patients with HCC, all receiving hormonal treatment with long-acting octreotide. All patients (n = 25) who received only treatment with long-acting octreotide were included in this retrospective comperative study.

Sections were slightly counterstained with Mayer’s hematoxylin and mounted in aqueous mounting medium (Glicergel, Dako). Dako control slides were used as positive controls and the negative control was performed by omitting the application of the primary antibody. IHC scoring was based on the membrane immunoreactivity, according to the American Joint

Committee [17]: 0, no reactivity, 1+, weak reactivity, 2+, moderate reactivity, 3+, strong reactivity. Chromogenic in situ hybridization Formalin fixed paraffin embedded (FFPE) sections were deparaffinized, dehydrated, AG-881 molecular weight air dried, and heated in boiling tissue heat pre-treatment buffer for 15 minutes using a SPoT-Light® FFPE reagent kit (Zymed, Histoline, Milan, Italy). Enzymatic digestion was performed using SPoT-Light® FFPE digestion enzyme (Zymed) for 2-3 minutes at RT. After dehydration, histological slides were air dried and the ready-to-use double-stranded DNA digoxygenin-labelled EGFR probe (Zymed) or the biotin labelled chromosome 7 centromeric probe (Zymed) were applied. Denaturation was performed by incubating the slides, covered with a CISH cover-slip, on a 96°C heating block for 5 minutes, and hybridization was performed by placing the slides in a humidity chamber at 37°C overnight. After removing the cover-slips, a stringent wash was performed in 0.5× saline-sodium citrate buffer

at 80°C for 5 minutes. The endogenous peroxidase activity and unspecific staining were blocked AZD5363 mw by applying 3% hydrogen peroxide and the CAS-Block™, respectively.

A mouse antidigoxygenin antibody was added to the slides hybridized with EGFR probe for 45 minutes at RT followed by incubation with a polymerized peroxidase-goat anti-mouse antibody (Dako) for 45 minutes at RT. On the FFPE tissue slides, the colorimetric signal of chromosome 7 centromeric probe was improved by incubating RG7420 chemical structure the slides with a mouse antibiotin antibody (Dako) for 45 minutes at 37°C. A DAB chromogen substrate system was used to generate a sensitive signal that could be viewed with a Nikon ECLIPSE 55i transmission light-brightfield microscope (Nikon, Amstelveen, The Netherlands) after Mayer’s haematoxylin counterstaining. Fluorescence in situ hybridization FISH was performed using the LSI EGFR (SpectrumOrange™), a locus-specific probe for the EGFR human gene locus (7q12) and the chromosome enumeration probe (CEP 7, SpectrumGreen™) for alpha-satellite DNA Vistusertib solubility dmso located at the centromere (7q11.1-q11.1) (Vysis, Inc., Downers Grove, IL). The assay was carried out according to the manufacturer’s instructions. Shortly after deparaffinization, the FFPE specimens were incubated in the pre-treatment solution (82°C, 30 minutes) and then digested with protease (37°C, 15 minutes). After washing, the slides were counterstained with 4′,6-diamidino-2 phenylindole (DAPI) and analyzed using a fluorescent microscope. An average of 30 nuclei was counted for each case.

This information is very useful to the physician when selecting the appropriate treatment before he receives the final identification from microbiological laboratory. Methods Reference microbial strains Several strains were used in the research: bacteria – Bacillus sp. (ATCC 51912), Enterobacter aerogenes (ATCC 29009), Enterococcus faecalis (ATCC 33186), Escherichia coli (ATCC 25922), Haemophilus this website influenzae (DSM 4690), Neisseria meningitidis (ATCC 53414), Proteus mirabilis (DSM 4479), Pseudomonas aeruginosa (DSM 13626), Serratia marcescens (DSM 50904),

Staphylococcus aureus (ATCC 33497), Staphylococcus epidermidis (ATCC 35983), Staphylococcus haemolyticus (DSM 20263), Streptococcus agalactiae (DSM 2134), Streptococcus pneumoniae (ATCC 49619), Streptococcus pyogenes (DSM 20565), Streptococcus Obeticholic Daporinad cost salivarius (DSM 20617), fungi – Aspergillus fumigatus (ATCC 14110), Candida albicans (ATCC 10231), Candida glabrata (DSM 11950), Candida parapsilosis (DSM 5784), Candida tropicalis (ATCC 20115). Ethics statement and participants The research was granted approval by the local Bioethics Committee of the Jagiellonian University (KBET/94/B/2009). Written informed consent

was obtained from participants before their enrollment in the study. Blood samples Blood was collected from volunteers, who had no clinical symptoms of sepsis and no inflammatory markers (CRP, OB). Additionally, 102 blood samples were taken from patients with clinical symptoms of sepsis, hospitalized in the John Paul

II Hospital in Krakow. Blood samples were drawn into 2-ml Vacutainer K3E (BectonDickinson) test tubes. Blood culture The blood culture was carried out in the John Paul II Hospital in Krakow in the Microbiology Department using BacT/ALERT® 3D apparatus (bioMérieux). DNA extraction of bacterial and fungal isolates The bacterial and fungal DNA was isolated with the application of a specialized kit for DNA extraction (Genomic Mini, DNA Gdansk). The isolation was carried out in accordance with the manufacturer’s report. The method for microbial DNA isolation from blood With the aim of determining the sensitivity of the PCR method, microbial DNA was isolated from 1.5-ml blood samples, collected old from volunteers, which were simultaneously inoculated with four model microbial reference strains (E. coli, S. aureus, C. albicans, A. fumigatus) in order to obtain a gradient of their number from 105 CFU/ml to 100 CFU/ml for each one of them. DNA isolation was carried out according to the method described by Gosiewski et al. with the employment of a ready-to-use Blood Mini (A&A Biotechnology) kit [4]. The same method was used to isolate DNA from blood samples of patients with clinical symptoms of sepsis. DNA purity and concentration The concentration and purity of total DNA isolates in the samples were measured spectrophotometrically at wavelengths of A 260 and A 280.

009). Table 2 Plasma pH and [HCO 3 - ] at rest and during cycle ergometer tests Sample pH HCO3 -(mmol/l)   ND LPVD ND LPVD PREdiet 7.467 ± 0.039 7.448 ± 0.028 33.6 ± 8.7 32.2 ± 6.0 POSTdiet 7.455 ± 0.028

7.454 ± 0.025 32.0 ± 5.5 31.9 ± 3.9 PREtest 7.466 ± 0.030 7.459 ± 0.015 32.9 ± 6.3 32.6 ± 4.5 Stage1 7.470 ± 0.029 7.473 ± 0.036 31.0 ± 3.1 31.7 ± 4.2 Stage2 7.459 ± 0.028 7.457 ± 0.031 28.6 ± 2.3 20.8 ± 3.3 CCI-779 solubility dmso Stage3 7.378 ± 0.039* 7.368 ± 0.029** 20.8 ± 3.3** 19.9 ± 2.2*** Stage4 7.326 ± 0.076* 7.336 ± 0.03*** 16.7 ± 2.5** 18.4 ± 2.4*** ND= normal diet. LPVD= low-protein vegetarian diet. PREdiet= a fasting blood sample taken in the morning before the start of ND or LPVD (day 1). POSTdiet= a fasting blood sample taken in the morning after a 4-day ND or LPVD (day 5). PREtest= a resting blood sample taken 30 min after a breakfast, before the cycle ergometer test (day 5). Stage1–4= blood samples taken after 10-min click here cycling at 40, 60 and 80% of VO2max and after the maximal stage (at 100% of VO2max until exhaustion). POSTdiet vs. Stage1–4 *= p<0.05; **= p<0.01; ***= p<0.001. Table 3 Independent variables of acid–base balance at rest and during cycle ergometer selleck chemicals llc tests Sample SID (mEq/l) Atot(mEq/l) pCO2(mmHg)   ND LPVD ND LPVD ND LPVD PREdiet 38.6 ± 1.8 38.6 ± 1.8 18.5 ± 0.8 18.3 ± 0.6 6.07 ± 1.29 6.13 ± 1.09 POSTdiet 39.4 ± 1.2 39.8 ± 0.9# 18.1 ± 1.0 18.1 ± 1.0 6.05 ± 0.82 5.98

± 0.64 PREtest 38.8 ± 1.5 38.5 ± 1.2* 18.1 ± 0.8 18.1 ± 1.0 5.98 ± 0.95 6.05 ± 0.89 Stage1 38.0 ± 1.1 37.9 ± 0.6** 18.8 ± 0.9 18.9 ± 0.5 5.60 ± 0.38 5.72 ± 0.97 Stage2 35.7 ± 1.0* 35.3 ± 1.7** 19.3 ± 0.8** 19.1 ± 0.8** 5.30 ± 0.28 5.27 ± 0.57

Stage3 30.6 ± 1.6** 29.5 ± 2.2*** 20.2 ± 1.0*** 20.1 ± 1.0** 4.61 ± 0.38* 4.55 ± 0.41** Stage4 29.6 ± 3.5** 29.1 ± 2.8*** 20.4 ± 1.5** 20.2 ± 1.0*** 4.23 ± 0.66* 4.51 ± 0.56** ND= normal diet. LPVD= low-protein vegetarian diet. PREdiet= a fasting blood sample taken Interleukin-3 receptor in the morning before the start of ND or LPVD (day 1). POSTdiet= a fasting blood sample taken in the morning after a 4-day ND or LPVD (day 5). PREtest= a resting blood sample taken 30 min after a breakfast, before the cycle ergometre test (day 5). Stage1–4= blood samples taken after 10-min cycling at 40, 60 and 80% of VO2max and after the maximal stage (at 100% of VO2max until exhaustion).

In Lactobacillus casei, high NaCl concentrations affect the size of bacterial cell and cell-wall modification, and the alteration of the cell wall increases antimicrobial susceptibility [40]. Although the genetic response of C. jejuni to high and low osmotic conditions has not been well studied yet, it has been reported that the rod spiral C. jejuni turns to coccoid forms when grown in nutrient media with low osmolality [34]. The previous report plus our findings demonstrate that both hyper- and hypo-osmotic stress abnormally

alters the morphology of C. jejuni. This may probably result from changes in intracellular ion concentrations by (de-)hydration under osmotic stress and may influence bacterial gene expression; however, understanding its molecular mechanisms still awaits further investigation. Cediranib cost The rpoN mutant was highly susceptible to acidic stress (pH 5.5) compared to wild type (Figure 3), whereas the growth of both the Ganetespib rpoN mutant and the wild type was similarly reduced under alkaline conditions (pH 8.5; Additional file 2, Figure S2A). Recently, an extensive screening of a transposon mutant library revealed that the adaptation of C. jejuni to acidic pH requires a number of genes mediating various cellular processes, including

those involved in motility, metabolism, stress response, DNA repair and surface polysaccharide biosynthesis [41]. Interestingly, mutations of motility-associated genes, such as flgR and fliD, impaired the growth of C. jejuni at low pH [41]. Based on this previous report, the AZD0156 order increased susceptibility to acid stress in the rpoN mutant may be associated with the motility defect of the rpoN mutant. Reactive oxygen species are inevitably produced by aerobiosis and cause damages to biomolecules, such as proteins, DNA and membranes [42]. As a microaerophile, C. jejuni requires oxygen for growth, though atmospheric level of oxygen is toxic to the cell. Various factors are known to mediate oxidative stress resistance in C. jejuni, including

SodB (superoxide dismutase), KatA (catalase), AhpC (alkyl hydroperoxide reductase), Dps (DNA-binding protein from starved cells), the multidrug efflux pump CmeG, Ribociclib molecular weight and PerR [43, 44]. In this work, the rpoN mutant was more resistant to H2O2 than the wild type, and complementation restored the H2O2 susceptibility to the wild-type level (Figure 4). This is similar to the case of PerR; the perR mutation increased C. jejuni’s resistance to H2O2 by derepressing katA [45]. It is unknown if RpoN is functionally related to PerR. However, the 16 RpoN-regulated genes which were predicted by in silico analysis in C. jejuni do not contain the oxidative stress resistance genes and perR [46]; thus, it appears that the change in H2O2 susceptibility by an rpoN mutation can be indirect in C. jejuni. It has been reported that the rpoN mutation makes the C. jejuni morphology less spiral [32, 33], suggesting RpoN affects the formation of the typical rod-spiral morphology of C. jejuni.

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