CrossRef 23. Liu RH, Yang J, Lenigk R, Bonanno J, Grodzinski P: Self-contained, fully integrated biochip for sample preparation, polymerase chain

reaction amplification, and DNA microarray detection. Anal Chem 2004,76(7):1824–1831.PubMedCrossRef 24. Quackenbush J: Microarray data normalization and transformation. Nat Genet 2002,32(Suppl):496–501.PubMedCrossRef 25. Stafford GP, Hughes C: Salmonella typhimurium flhE, a conserved flagellar regulon gene required for swarming. GSK126 molecular weight Microbiology 2007,153(Pt 2):541–547.PubMedCrossRef 26. Stoodley P, Lewandowski Z, Boyle JD, Lappin-Scott HM: The formation of migratory ripples in a mixed species bacterial biofilm growing in turbulent flow. Environ Microbiol 1999,1(5):447–455.PubMedCrossRef 27. Hot SDS/phenol RNA prep [http://​www.​biotech.​wisc.​edu/​Libraries/​GEC_​documents/​GEC_​RNA_​purification_​ecoli.​pdf] CB-839 Authors’ contributions DD carried out experimental studies and data analysis, participated in the design of the study, and drafted the manuscript. DH was involved in microarray data analysis and revising the manuscript. LR participated in the design of the study and revising the manuscript. CX conceived of the study, participated in its design and coordination, and revised the manuscript. All authors read and approved the final manuscript.”
“Background Salmonella enterica serovar Typhimurium

(S. Typhimurium) is a Gram-negative intracellular pathogen that causes gastroenteritis in the human host. Although non life-threatening in healthy adults, it can be fatal for children and immunocompromised individuals. The infection proceeds via two main stages: invasion and systemic

infection. During the invasion stage, the Tolmetin pathogen adheres and colonizes the intestines gaining access to the epithelial cells. Subsequently, Salmonella crosses the epithelial cells and gets internalized by the macrophages where it reproduces and stealthily spreads in the host and causes systemic infection [1–4]. Clearly, Salmonella must adapt quickly to the diverse environments it encounters. In fact, from the gastrointestinal tract to the intracellular milieu, it is challenged with fluctuations in oxygen concentration and with numerous host-immune defenses including a battery of reactive oxygen (ROS) and nitrogen species (RNS) and antimicrobial peptides that reduce its ability to colonize the host [1–4]. In Escherichia coli, ArcA (Aerobic Respiratory Control) is one of the main transcriptional regulators involved in the metabolic shift from anaerobic to aerobic LB-100 conditions and controlling the enzymatic defenses of bacteria against ROS. ArcA is a cytosolic response regulator of a two-component global regulatory system, ArcA/ArcB, where ArcB is a transmembrane histidine kinase sensor.

Only a few telomeric learn more proteins that bind the double-stranded form of telomeric DNA AP26113 nmr have been described in Leishmania and in their trypanosome counterparts [17, 23]. Homologues of human TRF have been found in the genomes of T. brucei, T. cruzi and L. major based on sequence similarities to the C-terminal Myb-like DNA binding domain. For example, the T. brucei TRF2 homologue known as TbTRF shares a similar telomere end-protection function with vertebrate TRF2 [24]. Results and Discussion Characterization of the putative L. amazonensis TRF gene homologue Using data mining via the

OmniBLAST server we searched the whole L. major genome database http://​www.​ebi.​ac.​uk/​parasites/​leish.​html Selleck BMN-673 for a putative sequence that shared similarities with the vertebrate TRF1 and TRF2 proteins. For this search, we used the most conserved part of both human proteins, the C-terminal fragment containing the Myb-like DNA binding domain. The search returned a single sequence

(GenBank acc. no. XP_001682531.1) that encoded a hypothetical protein (GenBank acc. no. Q4QDR7, GeneDB_Lmajor LmjF18.1250), the C-terminus of which shared ~30% identity and 50-55% similarity with the vertebrate TRF Myb-like domain, according to the blast2 sequence analysis (Table 1). Based on the L. major sequence, primers were designed for PCR amplification of the entire homologous sequence from L. amazonensis with genomic DNA as the template. PCR products of 2,931 bp were cloned into the vector pCR2.1 and both insert strands were sequenced (data not shown). The

deduced polypeptide sequence of 796 amino acid residues contained a putative C-terminal Myb-like DNA binding domain between 4-Aminobutyrate aminotransferase residues 684-733, according to psi-blast (Fig 1 – top). The LaTRF gene (GenBank acc. no. EF559263) shared high sequence identity and similarity to the putative L. major TRF, and to hypothetical L. infantum and L. braziliensis TRFs (Table 1). The sequence conservation between LaTRF and the trypanosome TbTRF and the putative TcTRF homologues decreased to 35-45% identity (Table 1), consistent with the known evolutionary relationships among these organisms. The Leishmania TRF homologues encode the largest TRF protein (~82.5 kDa) described so far. The fact that the Leishmania proteins showed much greater homology with each other than with other protozoan proteins and that they are the largest TRF described so far resembles the situation for Leishmania telomerase protein [25].

Ler promotes the expression of many H-NS-repressed SYN-117 virulence genes including those of LEE1-5, grlRA and non-LEE-encoded virulence genes such as lpf and the virulence plasmid pO157-encoded mucinase stcE[26, 28, 31, 36–39]. Thus, Ler antagonizes H-NS in the regulation of many virulence genes, which belong to both the H-NS and Ler (H-NS/Ler) regulons. The E. coli stringent starvation protein A (SspA) is a RNA polymerase-associated protein mTOR inhibitor cancer [40] that is required for transcriptional activation of bacteriophage P1 late genes and

is important for survival of E. coli K-12 during nutrient depletion and prolonged stationary phase [41–43]. Importantly, SspA down-regulates the cellular H-NS level during stationary phase, and thereby derepress the H-NS regulon including genes

for stationary phase induced acid tolerance in E. coli K-12 [44]. A conserved surface-exposed pocket of SspA is important for its activity as a triple alanine substitution P84A/H85A/P86A in surface pocket residues abolishes SspA activity [45]. SspA is highly conserved among Gram-negative pathogens [44], which suggests a role of SspA in bacterial pathogenesis. Indeed, SspA orthologs affect the virulence of Yersinia enterocolitica, Neisseria gonorrhoeae, Vibrio cholerae, Francisella tularensis and Francisella novicida[46–51]. Since E. coli K-12 SspA is conserved in EHEC where H-NS negatively Tanespimycin modulates virulence gene expression, we asked the question of whether SspA-mediated regulation of H-NS affects EHEC virulence gene expression. Here we study the effect of SspA on the expression of LEE- and non-LEE-encoded virulence genes and its effect on H-NS

accumulation in EHEC. Our results show that in an sspA mutant elevated levels of H-NS repress the expression of virulence genes encoding the T3SS system rendering the cells incapable of forming A/E lesions. 3-mercaptopyruvate sulfurtransferase Thus, our data indicate that SspA positively regulates stationary phase-induced expression of H-NS-controlled virulence genes in EHEC by restricting the H-NS level. Results and discussion SspA positively affects transcription of EHEC virulence genes To evaluate the effect of sspA on virulence gene expression in EHEC during the stationary phase we constructed an in-frame deletion of sspA in the E. coli O157:H7 strain EDL933 ATCC 700927 [52] and measured transcription of LEE- (LEE1-5, grlRA and map) and non-LEE-encoded (stcE encoded by pO157) genes (Figure  1). Wild type and sspA mutant strains were grown in LB medium to stationary phase with similar growth rates (data not shown). Total RNA was isolated and transcript abundance was measured by primer extension analyses using labeled DNA oligos specific to each transcript of interest and ompA, which served as internal control for total RNA levels.

Acknowledgements This work was supported by the Natural Science foundation of Jiangsu (grant number: BK20131439) and the Jiangsu Province Institute of Cancer Research Foundation (grant number: ZK201203) and the 2012 International Exchange Support Program of Jiangsu Health. References 1. Siegel R, Naishadham D, Jemal A: Cancer statistics, 2013. CA Cancer J Clin 2013,63(1):11–30.PubMedCrossRef 2. Yang L, et al.: Estimates of cancer incidence in China for 2000 and projections for 2005. Cancer Epidemiol Biomarkers Prev 2005,14(1):243–50.PubMed 3. Cannistra 4EGI-1 SA: Cancer

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selleckchem recurrent epithelial ovarian cancer. J Surg Oncol 2010,101(5):418–24.PubMed 6. Landoni F, et al.: Platin-based chemotherapy and salvage surgery in recurrent ovarian cancer following negative second-look find more laparotomy. Acta Obstet Gynecol Scand 1998,77(2):233–7.PubMedCrossRef 7. Boran N, et al.: Secondary cytoreductive surgery outcomes of selected patients with paclitaxel/platinum sensitive recurrent epithelial ovarian cancer. J Surg Oncol 2012,106(4):369–75.PubMedCrossRef 8. Chi DS, et al.: Guidelines and selection criteria for secondary cytoreductive surgery in patients with recurrent, platinum-sensitive epithelial ovarian carcinoma. Cancer 2006,106(9):1933–9.PubMedCrossRef 9. Bristow RE, Puri I, Chi DS: Cytoreductive surgery for recurrent ovarian cancer: a meta-analysis. Gynecol Oncol 2009,112(1):265–74.PubMedCrossRef 10. Harter P, et Sorafenib in vivo al.: Surgery in recurrent ovarian cancer: the Arbeitsgemeinschaft Gynaekologische Onkologie (AGO) DESKTOP OVAR trial. Ann Surg Oncol 2006,13(12):1702–10.PubMedCrossRef 11. Harter P, et al.: Surgery for recurrent ovarian cancer: role of peritoneal carcinomatosis: exploratory analysis of

the DESKTOP I Trial about risk factors, surgical implications, and prognostic value of peritoneal carcinomatosis. Ann Surg Oncol 2009,16(5):1324–30.PubMedCrossRef 12. Wang F, et al.: CA-125-indicated asymptomatic relapse confers survival benefit to ovarian cancer patients who underwent secondary cytoreduction surgery. J Ovarian Res 2013,6(1):14.PubMedCrossRef 13. Tian WJ, et al.: A risk model for secondary cytoreductive surgery in recurrent ovarian cancer: an evidence-based proposal for patient selection. Ann Surg Oncol 2012,19(2):597–604.PubMedCrossRef 14. Moertel CG, Hanley JA: The effect of measuring error on the results of therapeutic trials in advanced cancer. Cancer 1976,38(1):388–94.PubMedCrossRef 15. Therasse P, et al.: New guidelines to evaluate the response to treatment in solid tumors.

The previously analyzed isolates have been cloned using techniques that do not completely assure the source to be from a clonal cell line, FG4592 and unintentional mixing of different in vitro cultures may cause cross-contamination problems when growing cells in microbiological laboratories. Thus, utilization of the micromanipulation

technique rules out the risk of cross contamination since see more downstream analyses are performed on material from a single cell. In order to validate allelic sequence divergence at the single cell level of G. intestinalis, it is of substantial importance to initiate the PCR reaction with high quality template DNA, where DNA from all alleles is present due to the complex nature of the assay. If the sensitivity of the analysis is not high enough, sequences produced in downstream reactions may indicate false negatives where regions of one or several alleles may not be properly amplified and would thereby not display double peaks in the chromatograms. The implementation of DNAreleasy showed full efficiency in

the chromatograms produced from single trophozoites of the GS/M-H7 isolate. A freeze/thaw protocol, which was evaluated simultaneously also produced products in the nested PCR reaction in accordance selleck compound with Miller et al [19]. This method however, only produced one sequence out of five that allowed the discrimination of double peaks in the chromatograms (Table 1). The in vitro establishment

of viable assemblage B cysts (GS isolate) is highly inefficient Forskolin nmr (unpublished data), and therefore impeded the addition of a proper control for the purpose of verifying the presence of ASH in sequences generated from single Giardia cysts. DNAreleasy for DNA extraction was the only method sensitive enough to generate sequences where ASH could be detected when analyzing single trophozoites, therefore, two different DNAreleasy protocols provided by the manufacturer were assayed on the clinical cysts. Utilization of the long protocol indicated a higher proficiency in downstream PCR reactions (data not shown). ASH was seen on the single cell level in all DNAreleasy treated single cells of the GS/M isolate, thus verifying our hypothesis of the occurrence of ASH in single Giardia assemblage B parasites. Positions in the sequence on the tpi locus, that have earlier been highlighted as variable between different sub-assemblages or haplotypes of GS/M (Table 1) were here verified as double peaks, indicating sequence divergence in the different alleles in single Giardia cells. ASH also occurred at the single cell level in the majority of the cysts (21 out of 36 analyzed assemblage B cysts). However, the alignment of all sequences from a single patient sample did not result in the establishment of a consensus sequence.

The sample learn more was obtained from the Enteric Diseases Laboratory Branch, Center of Disease Control and Prevention (CDC, Atlanta, GA). Furthermore, 2 E. coli O104:H4 APO866 chemical structure strains 2050 and 2071, recovered from an outbreak in the Republic of Georgia, were also obtained from the CDC. Unless indicated, strains were grown overnight in Luria-Bertani (LB) medium at 37 °C, shaking at 225 rpm. The aerobactin transport iutA mutant CSS001 was constructed by PCR amplification and cloning of a fragment containing the iutA gene, disrupted with the cam cassette and cloned into the pCVD442 suicide vector. The mutagenesis approach was previously described [23]. The iutA mutant was confirmed

by PCR by using the oligonucleotides listed in Table 1, under the following conditions: 1 cycle at 94 °C for 3 min, and then 30 cycles at 94 °C for 1 min, 60 °C for 1 min, and 72 °C for 1 min. For the spatial-temporal location of E. coli O104:H4 in mice, the transformed RJC001 was constructed selleck kinase inhibitor by electroporation with 3 μg of pCM17 plasmid, containing the luxCDABE operon driven by the OmpC promoter (constitutive expression), which was previously used to visualize pathogenic E. coli[19]. The plasmid was generously donated by J.B. Kaper. Transformants were selected on LB agar plates supplemented with kanamycin (50 mg/ml), and BLI was confirmed by using the

IVIS Spectrum (Caliper Corp., Alameda, CA). Table 1 qRT-PCR primers used in this study Primer name Sequence Characteristics References 5RTRRSB 5’-TGCAAGTCGAACGGTAACAG-3’ qRT-PCR rrsb gene [40] 3RTRRSB 5’-AGTTATCCCCCTCCATCAGG-3’

rpoS Fw 5’-AGTCAGAATACGCTGAAAGTTCATG-3’ qRT-PCR BCKDHA rpoS gene [41] rpoS Rv 5’-AAGGTAAAGCTGAGTCGCGTC-3’ iutAFw 5’- GATCATAGTGTCTGCCAGCC-3’ qRT-PCR iutA gene This study iutARv 5’- GCTCTTTACCGCCCTGAATC-3’ iutAO104_F 5’-ATGGAGTTTGAGGCTGGCAC-3’ iutA mutant confirmation This study iutAO104_R 5’-GCTTACTGTCGCTGACGTTC-3’     Growth curves Cultures containing no antibiotics were grown overnight at 37 °C, 225 rpm. On the next day, 1:500 dilutions of overnight were inoculated into 30 mL of pre-warmed, sterile LB media. The growth of CSS001 was compared to the growth of wild-type E. coli O104:H4 strain C3493. Sampling was performed at approximately 1-h intervals during the first 9 h of the assay, and a final sample was analyzed 24 h from the start of the experiment. The growth of the E. coli wild- type and CSS001 strains was monitored by plating serial dilutions (log10 CFU/ml) from the time points on LB media with and without 2,2’-dipyridyl as well as by OD600 readings (Additional file 1: Figure S1). Mice Female ICR (CD-1) mice of 20 to 25 g were obtained from Charles River Laboratories and housed in the pathogen-free animal facility at UTMB upon arrival for 72 h prior to experiments. Animal studies were performed in accordance with the Animal Care and Use Committee’s guidelines at UTMB as recommended by the National Institute of Health.

When the mutant was complemented with pBAD24-tatABC, CT production of the N16961-dtatABC-cp strain increased compared to that of the mutant strains, N169-dtatABC and N169-dtatABC(pUC18) (P < 0.05 for the N16961-dtatABC-cp/N16961 comparison, and P < 0.05 for the N169-dtatABC-cp/N169-dtatABC comparison, One-Way ANOVA: Post Hoc Multiple Comparisons method, Fig. 6), indicating that the decrease in CT production in the

supernatant of the mutant may result from a defect in the Tat system. Figure 6 CT production in the supernatant of strains N16961, N169-dtatABC, and N169-dtatABC-cp. The strains were cultured find more using the AKI method. Data were obtained in independent triplicate cultures for each strain. We also measured the amount of CT in the cytoplasm. The CT concentration

in the cytoplasm of both N16961 and N169-dtatABC cells was much lower (< 5 ng/ml/OD600) than that in the culture supernatant (14–19 μg/ml/OD600), indicating that most of the CT was exported. The percentages of toxin secreted in the wild type strain and the tatABC mutant were nearly identical (99.97% and Crenigacestat molecular weight 99.93%, respectively). Although CT was still exported in the mutant, its production was markedly decreased compared to that of the wild type strain. We then examined CT gene transcription in the tat mutant and wild type strain with quantitative RT-PCR. We determined that, for the ctxB gene, the difference ΔΔCt of N169-dtatABC/N16961 was 1.523 with thyA as the internal reference and 1.506 with the 16S rDNA gene as the internal reference. Based on 2-ΔΔCt method, the ctxB gene transcription level of N169-dtatABC was 0.348 times compared to N16961 when using thyA as reference, and 0.352 times when using 16s-rDNA gene as reference, showing that cholera toxin gene was downregulated in the Tat mutant when compared to the wild type strain. In vivo colonization and

in vitro cell attachment experiments Colonization in the host intestine is required for the pathogenicity of V. cholerae. To analyze the colonization buy BMS-907351 ability of the tat mutant strain, science a suckling mouse intestine model was used in competitive experiments. We found that the colonization ability of the mutant was less than that of the wild type strain, as the colonization competitive ratio of the wild type strain N16961 to the mutant strain N169-dtatABC was 84:1 (from 40 to 120). Additionally, in the cell culture model, attachment to HT-29 was lower for the mutant than for the wild type strain (Fig. 7A to 7D). The attachment competitive ratio for the wild type strain N16961 to the mutant strain N169-dtatABC was 39: 1 (from 16 to 49). When the mutant strain was complemented with pTatABC-N16961, the attachment ability was restored (Fig. 7D). Figure 7 Colonization and attachment attenuation of the tatABC mutant N169-dtatABC. A.

CLSM examination of S. maltophilia Sm192 biofilm after 24 h of development. Orthogonal images, collected within the biofilm as indicated by the green and red lines in the top view, showed that biofilm consisted of cells forming a multilayered structure (red, propidium iodide-stained)

embedded in an abundant extracellular polymeric substance (blue, concanavalin A-stained). Image ON-01910 order capture was set for simultaneous visualization of both red and blue fluorescence. Magnification, ×100. Significant differences were also found among sequential isolates in some cases concerning susceptibility to oxidative stress (Sm194 vs Sm190, p < 0.05; Sm194 vs Sm192, p < 0.001) and swimming motility (Sm193 vs Sm194 and Sm195, p < 0.001) (data not shown). Swimming and twitching motilities are critical for biofilm development in CF strains Overall, 9 nonmotile strains, 4 non-CF strains and 5 CF strains, with neither swimming nor twitching motility were observed, with only 2 of them resulting in see more the inability to form biofilm. No significant differences were seen in motility, in the percentage of motile strains, and in the mean motility level between CF and non-CF isolates (data not shown). Similarly, among ENV isolates growth temperature did not significantly affect neither swimming nor twitching motility (data not shown).

Interestingly, swimming and twitching motilities were positively correlated to biofilm biomass (Pearson r: 0.528 and 0.625, respectively; p < 0.0001) in CF strains only. No statistically significant differences were found among the motility patterns (swimming+/twitching+, swimming+/twitching-, swimming-/twitching+, and swimming-/twitching-) with respect to the biofilm formed (data not shown). CF and non-CF isolates show comparable virulence in a mouse model of lung infection As shown in Figure 5A, a weight reduction Anacetrapib of at least 10% was observed on day 1 post-exposure (p.e.) in mice this website infected with invasive Sm46 and Sm188 strains and those exposed to non-CF Sm174, and later for mice exposed to CF strains (on day 2 and 3 p.e. for Sm122 and Sm111 strains, respectively). By day 1 p.e. the mean weight

of infected mice was significantly (p < 0.01) lower than that of control mice. By day 2 p.e., only infected mice with non-CF strains (Sm174, Sm170) and the invasive Sm188 strain slowly started regaining weight, although only mice infected with Sm170 strain regained it completely on day 3 p.e.. Control mice lost not more than 1% of their body weight during the study-period monitored. All infected mice showed symptoms of slow responsiveness and piloerection from day 1 through day 3 p.e.. Figure 5 Mouse model of acute lung infection by C F and non-CF S. maltophilia strains. DBA/2 mice (n = 8, for each strain) were exposed on day 0 to aerosolized CF (Sm111 and Sm122 strains, from respiratory specimens) or non-CF (Sm170 and Sm174 strains, from respiratory specimens; Sm46 and Sm188 strains, from blood) S. maltophilia in PBS.

5 Deaths Walden R. 1990 Plastic/* * 1/1 Yes Arterial embolization. Survived Missliwetz J. 1991 Plastic pellets 1 g/302 m/s/ 694J 4.5 4/1 Yes Soft tissue injury Survived Yellin A. 1992 Plastic 8.5 g/*/* * 26/26• Yes Lung contusion (18) rib fracture Temsirolimus solubility dmso (8), hemo-pneumothorax (6), cardiac injury (3) sternal fracture (1), scapula fracture (1), vascular injury (5), esophageal injury (1) 1 Death Hiss J. 1997 Rubber and steel/15.4 g/100 m/s/41.5 J and Plastic 0.85 g/1225 m/s/663.7 J * 17/2 Yes Lung and heart lacerations 2 Deaths Voiglio E.J 1998 Rubber pellets/*/* Contact

1/1 Yes Hemothorax, rib fracture, cardiac laceration. Died Chute DJ 1998 Plastic 79.4 g/74 m/s/220 J * 1/1 No Hemothorax, rib fracture, lung laceration, cardiac laceration Died Steele J.A 1999 Plastic 135 g/70 m/s/332 J * 155/25 * * All survived Mahajna A. 2002 Rubber Nutlin-3a mw 48 g/130 m/s/46 J and 17 g/78 m/s/33 J 30–80 152/39 Yes Lung contusion and rib fracture (8), pneumothorax (6), hemothorax (4), cardiac tamponade (1), cardiac contusion (1), vascular injury (1) All survived Kalebi A. 2005 Rubber pellets

*/*/* * 1/1 Yes Hemothorax, lung laceration, rib fracture Died Hughes D. 2005 Plastic 98 g/64 m/s/244 J * 28/7 No Lung contusion All survived Wahl P. 2006 Rubber 28 g/*/200 J 2 2/1 No Lung contusion, cardiac contusion Survived Maguire K. 2007 Plastic Crenolanib attenuated energy 28 g/*/200 J * 13/2 No Pneumothorax (1) Survived Chowaniec C. 2008 Rubber 8 g/94 m/s/40 J and pellets 0.3 g/215 m/s/7.3 J * 1/1 Yes Hemothorax, lung laceration, cardiac laceration Died Rezende-Neto J. 2009 Rubber attenuated energy 19 g/130 m/s/ 200 J 2

1/1 Yes Pneumothorax, lung laceration Survived Range in meters; * Missing information; ^children; • only patients with penetrating chest injuries were included in the study. When a projectile strikes a person, its kinetic energy at impact is defined by its mass and its velocity (1/2 × mass × velocity2). Ballistic studies suggest that a projectile needs to apply a “”threshold find more energy density”" of greater than 0.1 J/mm2 to skin in order to penetrate and cause internal injuries [5]. Manufacturers of rubber bullets modify the composition (mass: rubber vs lead), ballistic properties (velocity) and size (cross-sectional area) in order to reduce the likelihood of skin penetration. Furthermore, law-enforcement officers often have specific “”rules of engagement”" for using these types of munitions that further reduce the likelihood of penetration and serious injury; such rules include firing at distances over 40 meters and changing the point of aim to body regions where skin has increased elastic properties (lower anterior abdomen or thigh) to allow the energy to dissipate over a larger cross-sectional area [6]. One broad classification of “”less lethal”" impact munitions is direct versus indirect fire rounds.

J Infect Dis 2004,189(3):420–430.PubMedCrossRef 33. Huebner J, Wang Y, Krueger WA, Madoff LC, Martirosian G, Boisot S, GSK872 mw Goldmann DA, Kasper DL, Tzianabos AO, Pier GB: Isolation and chemical characterization of a capsular polysaccharide antigen shared by clinical isolates of Enterococcus faecalis and vancomycin-resistant Enterococcus faecium. Infect Immun 1999,67(3):1213–1219.PubMed 34. Callegan MC,

Jett BD, Hancock LE, Gilmore MS: Role of hemolysin BL in the pathogenesis of extraintestinal Bacillus cereus infection assessed in an endophthalmitis model. Infect Immun 1999,67(7):3357–3366.PubMed 35. Arnaud M, Chastanet A, Debarbouille M: New vector for efficient allelic replacement in naturally nontransformable, low-GC-content, gram-positive bacteria. Appl Environ Microbiol

2004,70(11):6887–6891.PubMedCrossRef LY2874455 datasheet Selleck GDC-941 Authors’ contributions CT participated in the isolation and TLC analysis of glycolipids and LTA, the design and interpretation of the experiments, made the statistical analysis, and drafted the manuscript. IS performed the cell culture assays, autolysis assay and hydrophobicity assay. YB carried out the biofilm assay and participated in the molecular genetic studies. AK performed the opsonophagocytic killing assay and the mouse infection model. PSC performed the biochemical analysis of glycolipids and LTA. EG participated in the draft of the manuscript. OH participated in the biochemical analysis of the glycolipids and LTA and the draft of manuscript. JH participated in the design, coordination and interpretation of the study, and the draft of the manuscript. All authors read and approved the final manuscript.”
“Background Multipartite genomes are common among members of the α-proteobacteria [1]. Most

symbiotic nitrogen-fixing bacteria belonging to the genera Rhizobium, Sinorhizobium, Mesorhizobium and Bradyrhizobium possess multipartite genomes organized as a single circular chromosome and a variable number of large plasmids [2]. In some species plasmids can represent, in terms of size, up to 40% of the total genome. In Rhizobium and Sinorhizobium species one plasmid (pSym) concentrates most of the genes required for nodulation and nitrogen Inositol oxygenase fixation [3]. The complete genome sequences of different rhizobia have revealed that plasmids harbor mainly accessory genes and that most encode predicted transport systems and a variety of catabolic pathways that may contribute to the adaptation of rhizobia to the heterogeneous soil and nodule environments [2, 4]. These genes are absent from closely related genomes, lack synteny and their G+C composition differs from that of the core genes. The core genes are mainly located on chromosomes, have essential functions in cell maintenance and have orthologs in related species [5, 6].