62 research outputs found

    Contribution of TAT System Translocated PhoX to Campylobacter jejuni Phosphate Metabolism and Resilience to Environmental Stresses

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    Campylobacter jejuni is a common gastrointestinal pathogen that colonizes food animals; it is transmitted via fecal contamination of food, and infections in immune-compromised people are more likely to result in serious long-term illness. Environmental phosphate is likely an important sensor of environmental fitness and the ability to obtain extracellular phosphate is central to the bacteria's core metabolic responses. PhoX is the sole alkaline phosphatase in C. jejuni, a substrate of the TAT transport system. Alkaline phosphatases mediate the hydrolytic removal of inorganic phosphate (Pi) from phospho-organic compounds and thereby contribute significantly to the polyphosphate kinase 1 (ppk1) mediated formation of poly P, a molecule that regulates bacterial response to stresses and virulence. Similarly, deletion of the tatC gene, a key component of the TAT system, results in diverse phenotypes in C. jejuni including reduced stress tolerance and in vivo colonization. Therefore, here we investigated the contribution of phoX in poly P synthesis and in TAT-system mediated responses. The phoX deletion mutant showed significant decrease (P<0.05) in poly P accumulation in stationary phase compared to the wild-type, suggesting that PhoX is a major contributor to the inorganic phosphate pool in the cell which is essential for poly P synthesis. The phoX deletion is sufficient for a nutrient stress defect similar to the defect previously described for the ΔtatC mutant. Additionally, the phoX deletion mutant has increased resistance to certain antimicrobials. The ΔphoX mutant was also moderately defective in invasion and intracellular survival within human intestinal epithelial cells as well as in chicken colonization. Further, the ΔphoX mutant produced increased biofilm that can be rescued with 1 mM inorganic phosphate. The qRT-PCR of the ΔphoX mutant revealed transcriptional changes that suggest potential mechanisms for the increased biofilm phenotype

    Platelet-rich plasma in orthopedic therapy: a comparative systematic review of clinical and experimental data in equine and human musculoskeletal lesions

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    Twisted Poincare duality for some quadratic Poisson algebras

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    We exhibit a Poisson module restoring a twisted Poincaré duality between Poisson homology and cohomology for the polynomial algebra R=C[X1Xn] endowed with Poisson bracket arising from a uniparametrised quantum affine space. This Poisson module is obtained as the semiclassical limit of the dualising bimodule for Hochschild homology of the corresponding quantum affine space. As a corollary we compute the Poisson cohomology of R, and so retrieve a result obtained by direct methods (so completely different from ours) by Monnier

    Differential Effects of Dimethylsulfoniopropionate, Dimethylsulfonioacetate, and Other S-Methylated Compounds on the Growth of Sinorhizobium meliloti at Low and High Osmolarities.

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    International audienceAn extract from the marine alga Ulva lactuca was highly osmoprotective in salt-stressed cultures of Sinorhizobium meliloti 102F34. This beneficial activity was due to algal 3-dimethylsulfoniopropionate (DMSP), which was accumulated as a dominant compatible solute and strongly reduced the accumulation of endogenous osmolytes in stressed cells. Synthetic DMSP also acted as a powerful osmoprotectant and was accumulated as a nonmetabolizable cytosolic osmolyte (up to a concentration of 1,400 nmol/mg of protein) throughout the growth cycles of the stressed cultures. In contrast, 2-dimethylsulfonioacetate (DMSA), the sulfonium analog of the universal osmoprotectant glycine betaine (GB), was highly toxic to unstressed cells and was not osmoprotective in stressed cells of wild-type strains of S. meliloti. Nonetheless, the transport and accumulation of DMSA, like the transport and accumulation of DMSP and GB, were osmoregulated and increased fourfold in stressed cells of strain 102F34. Strikingly, DMSA was not toxic and became highly osmoprotective in mutants that are impaired in their ability to demethylate GB and DMSA. Furthermore, 2-methylthioacetate and thioglycolic acid (TGA), the demethylation products of DMSA, were excreted, apparently as a mechanism of cellular detoxification. Also, exogenous TGA and DMSA displayed similar inhibitory effects in strain 102F34. Thus, on the basis of these findings and other physiological and biochemical evidence, we infer that the toxicity of DMSA in wild-type strains of S. meliloti stems from its catabolism via the GB demethylation pathway. This is the first report describing the toxicity of DMSA in any organism and a metabolically stable osmoprotectant (DMSP) in S. meliloti

    Association between rat decompression sickness resistance, transthyretin single nucleotide polymorphism, and expression: A pilot study

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    International audienceDecompression sickness (DCS) is a systemic syndrome that can occur after an environmental pressure reduction. Previously, we showed that the plasmatic tetrameric form of transthyretin (TTR) nearly disappeared in rats suffering DCS but not in asymptomatic ones. In this pilot study, we assessed whether the resistance to DCS could be associated with polymorphism of the gene of TTR. For this study, Sanger sequencing was performed on purified PCR products from the liver of 14‐week‐old male and female standard and DCS‐resistant rats ( n = 5 per group). Hepatic TTR mRNA expression was assessed by RT‐qPCR in 18–19 week‐old male and female standard and resistant rats ( n = 6 per group). There is a synonymous single nucleotide polymorphism (SNP) on the third base of codon 46 (c.138 C &gt; T). The thymine allele was present in 90% and 100% of males and females standard, respectively. However, this allele is present in only 30% of DCS‐resistant males and females ( p = 0.0002301). In the liver, there is a significant effect of the resistance to DCS ( p = 0.043) and sex ( p = 0.047) on TTR expression. Levels of TTR mRNA were lower in DCS‐resistant animals. To conclude, DCS resistance might be associated with a SNP and a lower expression of TTR
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