Int J Syst Evol Microbiol 1999, 49:1707–1715 10 Dore MP, Sepulv

Int J Syst Evol Microbiol 1999, 49:1707–1715. 10. Dore MP, Sepulveda AR, El-Zimaity H, Yamaoka Y, Osato MS, Mototsugu K, Nieddu AM, Realdi G, Graham DY: Isolation of Helicobacter pylori from sheep-implications for transmission to humans. Am J Gastroenterol 2001, 96:1396–1401.PubMed 11. Dimola S, Caruso ML: Helicobacter GSK126 mw pylori in animals affecting the human habitat through the food chain. Anticancer Res 1999, 19:3889–3894.PubMed 12. Contreras M, Morales A, Garcia-Amado MA, De Vera M, Bermudez V, Gueneau P: Detection of Helicobacter-like DNA in the gastric mucosa of Thoroughbred horses. Lett Appl Microbiol 2007, 45:553–557.PubMedCrossRef 13. Johnson B, Carlson GP, Vatistas NJ, Snyder JR, Lloyd K, Koobs

J: Investigation of the number and location of gastric ulcerations in horses in race training submitted to the California Racehorse postmortem program. Proceedings of the 40th Annual Convention of the Seliciclib in vivo American Association of Equine Practitioners 1994, 123–124. 14. Amann RI, Ludwig W, Schleifer KH: Phylogenetic identification and in situ detection of individual microbial cells without cultivation. Microbiol Rev 1995, 59:143–169.PubMed 15. Recordati C, Gualdi V, Craveb M, Sala L, Luini M, Lanzoni A, Rishniw M, Simpson KW, Scanziani learn more E: Spatial distribution of Helicobacter

spp. in the gastrointestinal tract of dogs. Helicobacter 2009, 14:180–191.PubMedCrossRef 16. Burton AB, Perkins GA, Parker J, Rosenthal R, Baumgart M, Simpson Niclosamide KW: The gastric mucosa of horses harbours an abundant and diverse bacterial flora [abstract]. Proceedings of American College of Veterinary Internal Medicine, Annual meeting, Seattle, WA, June 6–9 2007., 2007: 17. Niyogi SK: Shigellosis. Journal of Microbiology 2005, 43:133–143. 18. Farmer JJ, Fanning GR, Davis BR, Ohara CM, Riddle C, Hickmanbrenner FW, Asbury MA,

Lowery VA, Brenner DJ: Escherichia-Fergusonii and Enterobacter-Taylorae, 2 New Species of Enterobacteriaceae Isolated from Clinical Specimens. J Clin Microbiol 1985, 21:77–81.PubMed 19. Wragg P, La Ragione RM, Best A, Reichel R, Anjum MF, Mafura M, Woodward MJ: Characterisation of Escherichia fergusonii isolates from farm animals using an Escherichia coli virulence gene array and tissue culture adherence assays. Res Vet Sci 2009, 86:27–35.PubMedCrossRef 20. Mahapatra A, Mahapatra S, Mahapatra A: Escherichia fergusonii: an emerging pathogen in South Orissa. Indian J Med Microbiol 2005, 23:204.PubMedCrossRef 21. Sarker SA, Gyr K: Non-immunological defence mechanisms of the gut. Gut 1992, 33:987–993.PubMedCrossRef 22. Campbell-Thompson ML, Merritt AM: Gastric cannulation in the young horse: a new technique for studying gastric fluid secretion. Proceedings of the 2nd Annual Colic Research Symposium 1986, 120–122. 23. Dulphy JP, Martin-Rosset W, Dubroeucq H, Ballet JM, Detour A, Jailler M: Compared feeding patterns in ad libitum intake of dry forages by horses and sheep.

Culture media were changed every 4 to 6 days FISH analysis We cu

Culture media were changed every 4 to 6 days. FISH analysis We cultured BCR/ABL+ hemangioblasts from male CML patients (n = 12) and Y chromosome was detected using a probe (CEP Y Spectrum Red; Vysis, Downers Selleck MDV3100 Grove, IL) according to the manufacturer’s instructions. Normal cells showed 2 red abl signals and 2 green bcr signals. BCR/ABL+ hemangioblasts showed a single

red and a single green signal representing normal abl and bcr genes and the yellow signal representing fusion of abl and bcr genes. Fluorescence activated cell sorting (FACS) For immunophenotype analysis, expanded clonal cells were stained with antibodies against Flk1, CD29, CD31, CD34, CD44, CD45, CD105, (all from Becton Dickinson Immunocytometry Systems, Mountain View, CA). For intracellular antigen detection, cells were first fixed in 2% paraformaldehyde (Sigma) for 15 minutes at 4°C and permeabilized with 0.1% saponin (Sigma) for 1 hour at room temperature. Cells were washed

and labeled with fluorescein isothiocyanate (FITC) conjugated secondary goat antimouse, goat antirabbit, or sheep antigoat antibodies (Sigma), then washed and analyzed using a FACS Calibur flow cytometer (Becton https://www.selleckchem.com/products/pp2.html Dickinson, San Jose, CA). Mitogen proliferative assays check details Inmitogen proliferative assays, triplicate wells containing responder 1 × 105 MNCs were cultured with 50 g/ml PHA (Roche, USA) in a total

volume of 0.1 ml medium at 37°C in 5% CO2, and Flk1+CD31-CD34- MSCs were added on day 0. Irradiated Flk1+CD31-CD34- MSCs (30 Gy) were cocultured with the MNCs at different ratios (MSCs to MNCs = 1:2, 1:10, 1:100). Control wells contained only MNCs. Cultures were pulsed with 1 Ci/well [3H]-TdR (Shanghai Nucleus Research Institute, China) on day 2, and harvested 18 h laterwith a Tomtec (Wallac Inc., Gaithersburg, Vasopressin Receptor MD) automated harvester. Thymidine uptake was quantified using a liquid scintillation and luminescence counter (Wallac TRILUX). Mixed lymphocyte reaction assays (MLR) Blood mononuclear cells (MNCs) were prepared from normal volunteers’ peripheral blood by Ficoll-Paque density gradient centrifugation and suspended inRPMI 1640 medium supplemented with 10% (vol/vol) FCS, 2 mM l-glutamine,0.1 mM nonessential amino acids (Life Technologies, Grand Island, NY), 1 mM sodium pyruvate, 100 U/mL penicillin, Effect of MSCs on T cell cycle MSCs and MNCs were prepared as described before.

Drops of dense suspension of the F strain

Drops of dense suspension of the F strain NSC23766 cell line were planted as smears of increasing diameter. As shown in Figure 7c, up to a critical diameter, roughly corresponding to the outer diameter of the interstitial circle of a normal F colony, the cells could still coordinate their

actions towards a full-fledged colony, albeit not with a full success. If compared with the standard F pattern, the central navel always occupied the whole area of planting, leaving to the interstitial ring only the space remaining to the critical diameter. Should the diameter of planting reach (or exceed) this critical diameter, no room was left for the interstitial circle, and the body turned into a macula, as predicted by our formal model. Figure 7 Simulation of inoculum geometry effects. a. Encounters of rimmed colonies. Profiles of mature colonies (including quorum levels) in the first learn more generation after AP26113 price growth cessation. Inoculum position indicated by black dots. Colonies sharing the same substrate are smaller and reach maturity sooner than singletons, and develop a common rim if planted sufficiently close together. b. Effects of inoculum size in simulated plantings by dropping. Top – number of generations required to reach final colony size, bottom – diameter of distinct

colony parts depending on initial inoculum size. Note that the simulation marked by the arrow resulted only in an imperfect, shallow rim, and simulations with larger inocula yielded maculae without a distinctive rim. Simulation

parameters were as for colony 1 in Figure 6b, c. c. Experimentally observed dependence of colony proportions (at day 7) on area of Rebamipide planting. Increasing the planting area leads to the expansion of the red center at the expense of the interstitial circle. Above 10 mm of planting diameter (i.e. standard diameter of the circle; dashed line), the circle disappears totally, and the resulting body grows towards a macula. Discussion Highly structured bacterial bodies (mats, plaques, stromatolites, colonies, etc., containing astronomical amounts of cells belonging to hundreds of species) apparently represent the “”default”" way of living of most bacteria [25–34]. How do such bodies come into existence? Are they ad hoc contraptions, molded solely, or predominantly, by the external environment? A result from an ecological succession, a game played by well-trained players? Or, finally, may an analogy of ontogeny be assumed [23], similar to ontogeny in, e.g. mycobacteria, streptomycetes, slime molds, yeasts, or even plants or animals? Our experiments with a single clone or a pair of clones, each giving well-developed colonies with finite growth, may provide initial insight into the processes of bacterial body formation. Apparently, there exists an elaborated network of communicative signals mutually affecting bacterial bodies, so the first hypothesis can be safely dismissed.

All sequences were analyzed with RDP3 and GARD software to detect

All sequences were analyzed with RDP3 and GARD software to detect the recombinants. The analysis in silico displayed the recombinants and one parental

strain. B) The E protein gene from MEX_OAX_1656_05 was cloned in TOPO TAV4 to detect possible recombinants and/or the parental sequences. One parental sequence was detected in addition to one recombinant. The first task in this phylogenetic analysis was to determine the best model of nucleotide substitution for DENV-2 virus sequence evolution. This assignment was undertaken using the Model this website Selection test from DataMonkey online server [28, 29], which compares 201 models of DNA substitution. Our results demonstrated that the best model was TrN93 [30]. Accordingly, the most complex general time-reversible value was the best fit to the data (relative substitution rates of A↔C = 0.057, A↔G = 1, A↔T = 0.057, C↔G = 0.057, C↔T = 1, and G↔T = 0.057); the Ln likelihood = -4550.59; parameter count = 38;

and AIC = 9177.19. Finally, the estimated base composition was A = 0.340, C = 0.278, G = 0.225, and T = 0.157. Our analysis with RDP3 showed that the sequences of isolate MEX_OAX_1038_05 and MEX_OAX_1656_05 present statistical evidence of recombinants for GENECOV (P-Val = 2.467 × 10-2), BOOTSCAN (P-Val = 4.289 × 10-5), MAXCHI (P-Val = 1.438 × 10-5), CHIMERA (P-Val = 3.790 × 10-3), SISCAN (P-Val = 1.108 × 10-9), and O-methylated flavonoid 3SEQ (P-Val = 4.478 × 10-4), in two regions (Figure 2): the first breakpoints were located in 499nt and 512nt respectively; the second breakpoints were located in CP673451 cost 868nt and 826nt respectively, and the third breakpoint was located in 2239nt in both recombinants (Figure 2A, 2B respectively). In addition, the analysis with GARD confirmed the breakpoints and recombination data for find more maximum likelihood. This analysis

displayed the same site for the three breakpoints in both isolates: the first, second and third breakpoints were located in the nucleotides 498, 828 and 2226, respectively (Figure 2C). The recombinant regions were the intersection of prM-M structural gene to intersection of M-E structural genes and the second recombinant region started in the intersection of E-NS1 genes (Figure 2D). Interestingly, we found that the parental major strain was the non-recombinant clone MEX_OAX_1656_05_ C241 (obtained from the MEX_OAX_1656_05 isolate) and the minor parental strain was the Cosmopolitan genotype strain INDI_GWL_102_01 (accession number DQ448235). Figure 2 Recombination plots of structural gene regions from MEX_OAX_1038_05 and MEX_OAX_1656_05 sequences. A) BOOTSCAN plot analysis of the C(91)-prM-E-NS1(2400) gene sequences from the MEX_OAX_1038_05 isolate and the parental strains INDI_GWL102_01 and MEX_OAX_1656_05_C241.

parapsilosis strains induced the expression of chemotactic molecu

parapsilosis strains induced the expression of chemotactic molecules, in C188-9 chemical structure addition, DCs infected with lipase deficient yeast showed increased cell death which is known to be accompanied by the buy 17DMAG release of danger signals [25]. Consequently, we propose that DCs infected with lipase deficient yeast cells activate more robust immune response. Although both wild type

and lipase deficient C. parapsilosis induced strong, time-dependent activation of pro-inflammatory genes such as IL-1α, IL-6, TNF-α, and CXCL-8 in both DC types, lipase deficient yeast induced significantly higher gene expression of effector molecules. Since locally produced chemotactic factors are presumed to mediate the sequence of events leading to the infiltration of immune cells at inflammatory sites, local expression of pro-inflammatory mediators after contact with C. parapsilosis could have an initiator role in the attraction of additional immune cells to the sites of infection. This is supported by the fact that CXCL8 is one of the most potent neutrophil chemoattractants [26] that affects not only the recruitment Pitavastatin cost of neutrophils into the tissues but also modulates the ability of these neutrophils to cross epithelial barriers and to kill pathogens. In addition, TNF-α

enhances the fungicidal properties of neutrophils, promotes the adhesion of immune to endothelial cells and acts as a danger signal. Corresponding to this finding, we found that DCs infected with lipase deficient yeast cells displayed increased protease activity, which accompanies cell death and the release of danger signals. Finally, TNF-α, IL-1α and IL-6 are also implicated in the induction of antimicrobial peptide expression in epithelial cells [27]. Taken together,

the secretion of pro-inflammatory mediators and the release of danger signals by DCs as a response to C. parapsilosis may play a crucial role in the recruitment of immune cells into the sites of infection. Conclusions Our work shows that C. parapsilosis activates monocyte-derived DCs, as demonstrated by increased phagocytosis and killing of yeast cells and proinflammatory protein secretion. Moreover, we found that DCs infected with lipase deficient C. parapsilosis are functionally more potent relative NADPH-cytochrome-c2 reductase to DCs infected with wild type yeast cells, which suggests that lipase interferes with DC activation. This finding was unexpected because lipases of other pathogenic microorganisms are considered to be inducers of immune response, consequently one would have predicted a decreased activation phenotype in response to lipase deficient C. parapsilosis. The fact that this was not the case appears to result, at least in part, the DC activation is suppressed by the C. parapsilosis lipase. Further studies will be required to identify the defective anti-C. parapsilosis effector mechanisms that increase susceptibility to invasive candidiasis and to determine how C.

The urine of three hamsters was mixed for each infection period

The urine of three hamsters was mixed for each infection period. The total protein content of each sample was 20 μg. Each pattern of urinary protein was separated by pI (4–7), 12.5% acrylamide gel, and subsequently silver staining (A, B), or immunoblotting with anti-L. interrogans pAb was done (C, D). Arrows (D) show spots of 60 kDa that reacted with the polyclonal antibody at 7–8 days post-infection. Each experiment Endocrinology antagonist was repeated three times, and the representative data are shown in this figure.

Proteins with increased levels after Leptospira infection A total of 29 protein spots that had increased density after infection (Figure 3B) were selected and analyzed by LC/MS/MS analysis. Database analysis showed that these urinary proteins were albumin, alpha-1-antitrypsin, alpha-1-inhibitor III, angiotensinogen, apolipoprotein A-I, ceruloplasmin, haptoglobin, pancreatic trypsin 1, pregnancy protein 60 kDa, protease serine 1, transferrin, transthyretin, AMBP protein, vitamin D-binding protein and Cu/Zn superoxide dismutase (Table 1). Most of these proteins were serum proteins, which are this website usually detected in the urine of patients with renal PR-171 nmr failure. It is noteworthy that some of the leptospiral proteins were also identified as ABC transporter, 3-hydroxyacyl-CoA dehydrogenase

(HADH), chloride channel, and conserved hypothetical proteins in the urine (Table 2). Table 1 List of hamster proteins excreted in urine that had increased levels of expression during infection Spot no. Accession no.† Protein annotation MW (kDa) pI Urinary marker of diseases (Reference) 28 gi:110347564 ceruloplasmin isoform b [Mus musculus] 121872 5.53 Acute renal transplant rejection [29, 30] P-type ATPase 29 gi:83816939 alpha-1-inhibitor III [Rattus norvegicus] 165038 5.7 No reports 30, 32, 33, 38 gi:58585560 albumin [Microtus fortis fortis] 70261 5.91 Glomerular disease [31, 32], Diabetes mellitus type 2 [33] 31 gi:17046471 transferrin [Mus musculus]

78794 6.92 Glomerular disease [31, 32] 34 gi:68052028 Alpha-1-antitrypsin precursor 46019 5.55 Glomerular disease [32] 35 gi:191388 pregnancy protein 60 kDa 47574 8.53 No reports 36 gi:19705570 angiotensinogen [Rattus norvegicus] 52177 5.37 Chronic kidney disease [34] 37 gi:193446 vitamin D-binding protein [Mus musculus] 54647 5.26 Glomerular disease [31, 32] 39-41 gi:41019123 Haptoglobin precursor 39090 5.76 Glomerular disease [31, 32], Diabetes mellitus type 2 [33] 42 gi:2497695 AMBP protein precursor 39669 5.87 Diabetes mellitus type 2 [33, 35] 43-45, 48 gi:62899898 Apolipoprotein A-I precursor 30720 5.86 Glomerular disease [36] 46, 51, 52 gi:6981420 pancreatic trypsin 1 [Rattus norvegicus] 26627 4.71 Pancreatitis [31] 47, 49 gi:16716569 protease, serine, 1 [Mus musculus] 26802 4.75 No reports 50, 53, 54 gi:6981684 transthyretin [Rattus norvegicus] 15852 5.

In contrast, the membrane-bound FtsH protease was only detected i

In contrast, the membrane-bound FtsH protease was only detected in the membrane fraction of both strains analyzed (not shown). Taken together, these results showed that cells displaying increased expression of σF-dependent genes accumulate this sigma factor in the cytoplasm. Figure 6 Subcellular localization of σ F . Immunoblot assays GDC-0973 mw performed with membrane and soluble fractions obtained from parental strain NA1000 (WT) and a CC3252 mutant with both cysteine residues

C131 and C181 replaced for serine (C131-181S). Aliquots were taken immediately before or after cells were treated with 55μM potassium dichromate (K2Cr2O7) for 30min. Membrane and soluble fractions were obtained as described in Methods. buy Idasanutlin Blots were developed using anti-σFantiserum and see more fluorescent CF680 Goat Anti-Rabbit IgG. σF is shown by an arrow. Neither σF nor σF-dependent genes CC2906 and

CC3255 are essential for Caulobacter resistance to metal stress To investigate the requirement of sigF for resistance of C. crescentus cells to dichromate or cadmium, the sensitivity of the parental strain and the sigF deletion mutant to exposure to these metals was monitored. Both strains displayed similar sensitivity profile to dichromate or cadmium (data not shown), suggesting that sigF is not essential for bacterial survival under this stress condition. As the deduced protein sequences of CC2906 and CC3255 are highly similar, we constructed a single deletion mutant strain in each gene (SG19 and SG20) as well as a double mutant (SG21) and tested the resistance of these strains to the metal stresses. Similar to what was found for the sigF deletion mutant, no increased sensitivity was observed for these mutant strains following RVX-208 exposure to either dichromate or

cadmium, when compared to parental cells (data not shown). Together, these data suggest that σF-mediated transcriptional response to chromium or cadmium is not essential for survival of C. crescentus to exposure to these metal ions. Discussion In this report, we clearly show that C. crescentus σF is involved in the transcriptional response to chromium and cadmium in an oxidative stress independent manner. Transcriptome analysis of cells under dichromate stress revealed that σF controls a small regulon comprised of eight genes, which are distributed in three transcriptional units. Although a conserved domain was predicted for the deduced protein sequence of all σF-dependent genes, only two of these sequences could be assigned to a possible function. The protein encoded by CC2748 belongs to the group of sulfite oxidases, which catalyze the oxidation of the toxic and very reactive sulfite to the inert sulfate anion [22]. The product of CC3257 is a member of the DoxX family.

Similarly, in our study too, most of the EPEC were of atypical va

Similarly, in our study too, most of the EPEC were of atypical variety and were of non-traditional serotypes. A future study in Kuwait should address whether atypical EPEC are associated with persistent diarrhoea. The majority of children in our study had nonbloody diarrhoea. Even those children find more who had EIEC or EHEC detected in their stools, did not present with bloody diarrhoea. It has been reported that in some cases, these infections do not result in bloody diarrhoea [26]. Intimin is the outer membrane protein of EPEC that mediates tight attachment

between the bacterium and the intestinal mucosa. We investigated the intimin subtypes of EPEC. There were eight subtypes and the most prevalent subtypes were β and θ. These were also the most frequently identified subtypes in

other studies [6, 7, 24]. Antimicrobial susceptibility studies of DEC showed that resistance to older antimicrobials such as ampicillin, NVP-BSK805 tetracycline and trimethoprim was appreciable and that multi-resistance (resistance to ≥ 3 antimicrobials) was present in 43.1% of the isolates. The resistance rates of DEC to different antimicrobial agents have varied in different studies. In the study in Tehran, Iran, a high prevalence of resistance to above three antimicrobial agents as in Kuwait was observed [15]. In the study in Tunis, Tunisia, a high prevalence of resistance to tetracycline and β-lactams was seen [16]. In ETEC isolates studied in Egypt, a high prevalence of Isoconazole resistance CP-690550 cell line to ampicillin, trimethoprim and tetracycline was seen; 28% of isolates showed multi-resistance; and resistance to other antimicrobials was rare [27]. In Mexico, resistance rates to ampicillin, tetracycline and trimethoprim were high and multi-resistance was 62%; there

was no resistance to ciprofloxacin and cefotaxime [28]. In Vietnam, resistance rates to ampicillin, trimethoprim and chloramphenicol exceeded 75% with 90% of all strains multi-resistant. Resistance to ciprofloxacin and imipenem was negligible [29]. A total of six E. coli isolates were resistant to a third-generation cephalosporin, cefotaxime. All of them were ESBL producers and possessed one or more genetic elements related to ESBL production. Five isolates had ISEcp1 element that is responsible for mobilization of bla genes [30]. There are very few reports of ESBL production by DEC [31–33]. DEC isolates in these studies were found to harbor blaCTX-M [31–33], blaTEM [32, 33] or blaPER genes [33]. In Kuwait, children with invasive diarrhea are normally treated with third generation cephalosporins. It is interesting that some of our DEC isolates were resistant to cefotaxime. Therefore, the prevalence of resistance to third generation cephalosporins should be continuously monitored to detect any increase in resistance rate that could affect treatment with this class of antibiotics. Our study has shown that all five categories of DEC reported from other parts of the world were also present in diarrhoeal children in Kuwait.

1 A pipet tip dipped into the suspension was used to stab the ce

1. A pipet tip dipped into the suspension was used to stab the center of a MH motility plate (0.4% agar). The plates were incubated at 37°C and the

diameter of the motility zone was measured every 12 h. Adherence/Invasion/Intracellular survival assay A gentamicin protection assay [34, 55] was used to assess RG7112 concentration the ability of 81–176, 81–176cj0596, and 81–176cj0596 + to adhere to, invade, and survive within INT407 human intestinal epithelial cells. Selleck SCH727965 Briefly, bacteria were grown in biphasic [brain heart infusion (BHI)/1% yeast extract (YE)] cultures at 37°C under microaerobic conditions for ~20 h. Bacteria were harvested, resuspended in phosphate buffered saline (PBS), then added in triplicate to semi-confluent INT407 cell monolayers (~1 × 105 cells/well) at a multiplicity of infection (MOI) of ~40:1 (bacteria:epithelial cells). The number of bacteria added was quantified by determination of CFU/mL. The cells were incubated

for 3 h at 37°C under microaerobic conditions and were washed with Hanks’ Balanced Salt Solution (HBSS), lysed with Triton X-100 and the number of adherent bacteria was quantified by viable counts. For determination of invasion, cells were incubated for 3 h with bacteria and then gentamicin was added to a final concentration of 250 μg/ml to kill any extracellular bacteria. After an additional 2 h of incubation, the cells were washed, lysed with Saracatinib order Triton X-100 and intracellular bacteria were quantified by viable counts. The gentamicin and Triton X-100 MICs of the three strains were also determined. For determination Venetoclax purchase of intracellular survival, the cells were incubated for 3 h with bacteria, 2 h with gentamicin, and then the INT407 cells were washed and incubated for 4 h in minimal essential media containing 3% fetal bovine serum and gentamicin (10 μg/ml) as described by Candon et al. [56]. After the incubation period, cells were washed and lysed with Triton-X 100 and the number of bacteria that survived intracellularly was quantified by viable counts. Mouse Colonization Experiments The in vivo relevance of Cj0596 was investigated by testing the ability of 81–176, 81–176cj0596, and 81–176cj0596

+ to colonize mice as described [34, 57, 58]. 10-week old female BALB/c-ByJ mice were given 500 μl of 5% sodium bicarbonate by oral gavage to neutralize stomach acid. The mice were then given a dose of 1 × 109 CFU in 500 ml of BHI/1% YE broth by oral gavage. Because there was an observed discrepancy between OD600 and CFU for the mutant (see Results), we first performed pilot experiments correlating OD600 and CFU for all of the strains. After four repetitions, we found the mutant OD600 that gave the same number of CFU as for the WT and revertant strain, and this is what we used for the mouse inocula. We also verified that each mouse received equal CFU by plating the inocula for viable counts at the time of inoculation.

8 Holden PA, Halverson LJ, Firestone MK: Water stress effects on

8. Holden PA, Halverson LJ, Firestone MK: Water stress effects on toluene biodegradation by Pseudomonas putida . Biodegradation 1997, 8:143–151.PubMedCrossRef 9. Potts M: Desiccation tolerance of prokaryotes. Microbiol Rev 1994, 58:755–805.PubMed 10. Csonka LN: Physiological and genetic responses of bacteria to osmotic stress. Microbiol Rev 1989, 53:121–147.PubMed 11. Papendick RI, Campbell GS: Theory and measurement of water potential. In Water Potential Relations in Soil Microbiology. SSA Special Publication Number 9. Edited by: Parr JF,

Gardner WR, selleck kinase inhibitor Elliot LF. Madison: Soil Science Society of America; 1981:1–22. 12. Welsh DT: Ecological significance of compatible solute accumulation by microorganisms: from single cells to global KU55933 clinical trial climate. FEMS Microbiol Rev 2000, 24:263–290.PubMedCrossRef 13. Halverson LJ, Firestone MK: Differential

effects of permeating and nonpermeating solutes on the fatty acid composition of Pseudomonas putida . Appl Environ Microbiol 2000, 66:2414–2421.PubMedCrossRef 14. Roberson EB, Firestone MK: Relationship between desiccation and exopolysaccharide production in a soil Pseudomonas sp. Appl Environ Microbiol 1992, 58:1284–1291.PubMed 15. Lloret J, Bolanos L, Mercedes Lucas M, Peart JM, Brewin MJ, Bonilla I, Rivilla R: Ionic stress and osmotic pressure induce different alterations in the lipopolysaccharide of a Rhizobium meliloti strain. Appl Environ Microbiol 1995, 61:3701–3704.PubMed 16. van de Mortel M, Halverson LJ: Cell envelope components contributing to biofilm growth and Verubecestat price survival of Pseudomonas putida in low-water-content habitats. Mol Microbiol 2004, 52:735–750.PubMedCrossRef 17. Steuter AA, Mozafar A, Goodin JR: Water potential of aqueous polyethylene glycol. Plant Physiol 1981, 67:64–67.PubMedCrossRef 18. Heipieper HJ, Meulenbeld G, van Oirschot Q, de Bont JAM: Effect of environ-mental factors on the trans / cis ratio of unsaturated fatty acids in Pseudomonas putida S12. Appl Environ Microbiol 1996, 62:2773–2777.PubMed 19. Kets EPW, de Bont JAM, Heipieper HJ: Physiological response of Pseudomonas putida

S12 subjected to reduced water activity. FEMS Microbiol Lett 1996, 139:133–137. Bcl-w 20. Steil L, Hoffmann T, Budde I, Volker U, Bremer E: Genome-wide transcription profiling analysis of adaptation of Bacillus subtilis to high salinity. J Bacteriol 2003, 185:6358–6370.PubMedCrossRef 21. Liu Y, Gao W, Wang Y, Wu L, Liu X, Yan T, Alm E, Arkin A, Thompson DK, Fields MW, Zhou J: Transcriptome analysis of Shewanella oneidensis MR-1 in response to elevated salt concentrations. J Bacteriol 2005, 187:2501–2507.PubMedCrossRef 22. Domínguez-Ferreras A, Pérez-Arnedo R, Becker A, Olivares J, Soto MJ, Sanjuán J: Transcriptome profiling reveals the importance of plasmid pSymB for osmoadaptation of Sinorhizobium meliloti . J Bacteriol 2006, 188:7617–7625.PubMedCrossRef 23.