Relevant bibliographies by topics / Bacterial metabolism and pathogenesis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Bacterial metabolism and pathogenesis'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Bacterial metabolism and pathogenesis"

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Xiong, Lifeng, Jade Teng, Michael Botelho, Regina Lo, Susanna Lau, and Patrick Woo. "Arginine Metabolism in Bacterial Pathogenesis and Cancer Therapy." International Journal of Molecular Sciences 17, no. 3 (March 11, 2016): 363. http://dx.doi.org/10.3390/ijms17030363.

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Das, Mayashree, Arshiya Dewan, Somnath Shee, and Amit Singh. "The Multifaceted Bacterial Cysteine Desulfurases: From Metabolism to Pathogenesis." Antioxidants 10, no. 7 (June 23, 2021): 997. http://dx.doi.org/10.3390/antiox10070997.

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Living cells have developed a relay system to efficiently transfer sulfur (S) from cysteine to various thio-cofactors (iron-sulfur (Fe-S) clusters, thiamine, molybdopterin, lipoic acid, and biotin) and thiolated tRNA. The presence of such a transit route involves multiple protein components that allow the flux of S to be precisely regulated as a function of environmental cues to avoid the unnecessary accumulation of toxic concentrations of soluble sulfide (S2−). The first enzyme in this relay system is cysteine desulfurase (CSD). CSD catalyzes the release of sulfane S from L-cysteine by converting it to L-alanine by forming an enzyme-linked persulfide intermediate on its conserved cysteine residue. The persulfide S is then transferred to diverse acceptor proteins for its incorporation into the thio-cofactors. The thio-cofactor binding-proteins participate in essential and diverse cellular processes, including DNA repair, respiration, intermediary metabolism, gene regulation, and redox sensing. Additionally, CSD modulates pathogenesis, antibiotic susceptibility, metabolism, and survival of several pathogenic microbes within their hosts. In this review, we aim to comprehensively illustrate the impact of CSD on bacterial core metabolic processes and its requirement to combat redox stresses and antibiotics. Targeting CSD in human pathogens can be a potential therapy for better treatment outcomes.
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Kirthika, Perumalraja, Khristine Kaith Sison Lloren, Vijayakumar Jawalagatti, and John Hwa Lee. "Structure, Substrate Specificity and Role of Lon Protease in Bacterial Pathogenesis and Survival." International Journal of Molecular Sciences 24, no. 4 (February 8, 2023): 3422. http://dx.doi.org/10.3390/ijms24043422.

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Proteases are the group of enzymes that carry out proteolysis in all forms of life and play an essential role in cell survival. By acting on specific functional proteins, proteases affect the transcriptional and post-translational pathways in a cell. Lon, FtsH, HslVU and the Clp family are among the ATP-dependent proteases responsible for intracellular proteolysis in bacteria. In bacteria, Lon protease acts as a global regulator, governs an array of important functions such as DNA replication and repair, virulence factors, stress response and biofilm formation, among others. Moreover, Lon is involved in the regulation of bacterial metabolism and toxin–antitoxin systems. Hence, understanding the contribution and mechanisms of Lon as a global regulator in bacterial pathogenesis is crucial. In this review, we discuss the structure and substrate specificity of the bacterial Lon protease, as well as its ability to regulate bacterial pathogenesis.
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Abuawad, Alaa. "Treatment of Macrophages with Gram-Negative and -Positive Bacterial Secretomes Induce Distinct Metabolic Signatures." Jordan Journal of Pharmaceutical Sciences 16, no. 2 (July 24, 2023): 465. http://dx.doi.org/10.35516/jjps.v16i2.1508.

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Infectious diseases represent major health and economic challenges globally. Emergence of multiple drug-resistant bacteria in the community and hospital has become a worldwide concern that requires novel approaches for rapid diagnosis and treatment. Metabolomics approach is a powerful tool providing important chemical information about the cellular phenotype of living systems, and the changes in their metabolic pathways in response to various perturbations. Metabolomics has become an important tool to study host-pathogen interactions and to discover potential novel therapeutic targets. In this study, untargeted LC-MS metabolic profiling was applied to differentiate between the impact of the secretome of the Gram-positive S. aureus SH1000 and Gram-negative P. aeruginosa PAO1 bacterial pathogens on THP-1 macrophages. The results showed that S. aureus and P. aeruginosa secretome affected alanine, aspartate and glutamate metabolism; sphingolipid metabolism; glycine and serine metabolism; GL metabolism; and tryptophan metabolism with different trends in THP-1 macrophages. However, the impact of both bacterial secretome on arginine and proline metabolism was similar. These data could contribute to a better understanding of pathogenesis and resistance of these bacteria and could pave the way for developing new therapeutics that selectively targeting Gram-positive or Gram-negative bacteria.
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Chen, Jiezhong, and Luis Vitetta. "Gut Microbiota Metabolites in NAFLD Pathogenesis and Therapeutic Implications." International Journal of Molecular Sciences 21, no. 15 (July 23, 2020): 5214. http://dx.doi.org/10.3390/ijms21155214.

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Gut microbiota dysregulation plays a key role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) through its metabolites. Therefore, the restoration of the gut microbiota and supplementation with commensal bacterial metabolites can be of therapeutic benefit against the disease. In this review, we summarize the roles of various bacterial metabolites in the pathogenesis of NAFLD and their therapeutic implications. The gut microbiota dysregulation is a feature of NAFLD, and the signatures of gut microbiota are associated with the severity of the disease through altered bacterial metabolites. Disturbance of bile acid metabolism leads to underactivation of bile acid receptors FXR and TGR5, causal for decreased energy expenditure, increased lipogenesis, increased bile acid synthesis and increased macrophage activity. Decreased production of butyrate results in increased intestinal inflammation, increased gut permeability, endotoxemia and systemic inflammation. Dysregulation of amino acids and choline also contributes to lipid accumulation and to a chronic inflammatory status. In some NAFLD patients, overproduction of ethanol produced by bacteria is responsible for hepatic inflammation. Many approaches including probiotics, prebiotics, synbiotics, faecal microbiome transplantation and a fasting-mimicking diet have been applied to restore the gut microbiota for the improvement of NAFLD.
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Bongaerts, Ger P. A., and David M. Lyerly. "Role of bacterial metabolism and physiology in the pathogenesis ofClostridium difficiledisease." Microbial Pathogenesis 22, no. 4 (April 1997): 253–56. http://dx.doi.org/10.1006/mpat.1996.0119.

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Enany, Shymaa. "Impact of Low pH on Microbial Growth Rate, ATP Production, and NADH to NAD+ ratio." Egyptian Journal of Medical Microbiology 29, no. 3 (July 1, 2020): 121–28. http://dx.doi.org/10.51429/ejmm29314.

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Background: Bacterial metabolism is the tendency of bacteria to live, function, and replicate fittingly under their current culture and varied environment conditions. Microorganisms have intricated metabolic regulatory mechanisms to ameliorate environmental stresses. Objectives: We examined the effect of acidic pH, as one of stresses, on growth rate and metabolism of five different microorganisms. Methodology: ATP level, as an indicator for microbial viability, and alterations in NADH/NAD+ ratio, which plays a critical role in microbial metabolism, were assessed. Results: Our results showed that alterations in pH influence metabolism of different bacterial species with different extent. The growth rate of Pseudomonas aeruginosa, Escherichia coli and Bacillus Subtilis were diminished with an elevation in ATP and NADH/NAD+ ratio at low pH. Contrary, MRSA and MSSA showed trivial alterations for ATP and NADH/NAD+ ratio. Conclusion: Ultimately, this study affirmed differences in metabolism between different species and confirmed that alterations in pH influenced the metabolism and hence the pathogenesis.
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Sumner, Sarah E., Rachel L. Markley, and Girish S. Kirimanjeswara. "Role of Selenoproteins in Bacterial Pathogenesis." Biological Trace Element Research 192, no. 1 (September 5, 2019): 69–82. http://dx.doi.org/10.1007/s12011-019-01877-2.

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Laborda-Illanes, Aurora, Lidia Sanchez-Alcoholado, María Emilia Dominguez-Recio, Begoña Jimenez-Rodriguez, Rocío Lavado, Iñaki Comino-Méndez, Emilio Alba, and María Isabel Queipo-Ortuño. "Breast and Gut Microbiota Action Mechanisms in Breast Cancer Pathogenesis and Treatment." Cancers 12, no. 9 (August 31, 2020): 2465. http://dx.doi.org/10.3390/cancers12092465.

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In breast cancer (BC) the employment of sequencing technologies for metagenomic analyses has allowed not only the description of the overall metagenomic landscape but also the specific microbial changes and their functional implications. Most of the available data suggest that BC is related to bacterial dysbiosis in both the gut microenvironment and breast tissue. It is hypothesized that changes in the composition and functions of several breast and gut bacterial taxa may contribute to BC development and progression through several pathways. One of the most prominent roles of gut microbiota is the regulation of steroid-hormone metabolism, such as estrogens, a component playing an important role as risk factor in BC development, especially in postmenopausal women. On the other hand, breast and gut resident microbiota are the link in the reciprocal interactions between cancer cells and their local environment, since microbiota are capable of modulating mucosal and systemic immune responses. Several in vivo and in vitro studies show remarkable evidence that diet, probiotics and prebiotics could exert important anticarcinogenic effects in BC. Moreover, gut microbiota have an important role in the metabolism of chemotherapeutic drugs and in the activity of immunogenic chemotherapies since they are a potential dominant mediator in the response to cancer therapy. Then, the microbiome impact in BC is multi-factorial, and the gut and breast tissue bacteria population could be important in regulating the local immune system, in tumor formation and progression and in therapy response and/or resistance.
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Prudhomme, N., R. Pastora, B. Muselius, M. D. McLean, D. Cossar, and J. Geddes-McAlister. "Exposure of Agrobacterium tumefaciens to agroinfiltration medium demonstrates cellular remodelling and may promote enhanced adaptability for molecular pharming." Canadian Journal of Microbiology 67, no. 1 (January 2021): 85–97. http://dx.doi.org/10.1139/cjm-2020-0239.

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Agroinfiltration is used to treat plants with modified strains of Agrobacterium tumefaciens for the purpose of transient in planta expression of genes transferred from the bacterium. These genes encode valuable recombinant proteins for therapeutic or industrial applications. Treatment of large quantities of plants for industrial-scale protein production exposes bacteria (harboring genes of interest) to agroinfiltration medium that is devoid of nutrients and carbon sources for prolonged periods of time (possibly upwards of 24 h). Such conditions may negatively influence bacterial viability, infectivity of plant cells, and target protein production. Here, we explored the role of timing in bacterial culture preparation for agroinfiltration using mass spectrometry-based proteomics to define changes in cellular processes. We observed distinct profiles associated with bacterial treatment conditions and exposure timing, including significant changes in proteins involved in pathogenesis, motility, and nutrient acquisition systems as the bacteria adapt to the new environment. These data suggest a progression towards increased cellular remodelling over time. In addition, we described changes in growth- and environment-specific processes over time, underscoring the interconnectivity of pathogenesis and chemotaxis-associated proteins with transport and metabolism. Overall, our results have important implications for the production of transiently expressed target protein products, as prolonged exposure to agroinfiltration medium suggests remodelling of the bacterial proteins towards enhanced infection of plant cells.
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Dissertations / Theses on the topic "Bacterial metabolism and pathogenesis"

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Haque, Md Risat Ul. "Bacterial nitric oxide metabolism in the pathogenesis of meningococcal sepsis." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/12201/.

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Neisseria meningitidis is the causative agent of fatal meningococcal sepsis in humans, characterised by high bacterial loads in blood, and collapse of the microcirculatory system. The organism is adapted to colonise the human nasopharynx, an environment which is oxygen poor but rich in nitric oxide (NO), a gas vital for the regulation of essential physiological processes such as vasorelaxation, antimicrobial and innate immune responses by the host. Furthermore, during sepsis caused by meningococcaemia, high concentrations of nitrite can be measured in the blood, derived from activated circulating monocytes and endothelial cells. Meningococci express a partial denitrification pathway comprising of a nitrite reductase (AniA) and a nitric oxide reductase (NorB) to survive and thrive in an oxygen deficient niche such as the nasopharynx. The aniA and norB genes are negatively regulated by an NO sensitive repressor, NsrR. Studies from our group have shown that NorB is critical for counteracting the antimicrobial and innate immune response of the host. As NO based regulation requires a tightly regulated equilibrium, this could have far reaching consequences on the NO mediated signalling processes, and is likely to be relevant to survival of the organism within NO-enriched nasopharyngeal mucosae and blood. Previously, it was shown that bacterial NO detoxification reduces the concentration of host-cell S-nitrosothiol (SNO), a vital post-translational modification akin to phosphorylation, in murine macrophages in vitro. To investigate if similar meningococcal NO metabolism mediated SNO depletion persists in vivo, we established a murine model of early acute meningococcal sepsis. We showed that bacterial burden correlates positively with plasma SNO and hepatic NO2- but negatively with hepatic NOx. However, bacterial NO metabolism did not differentially modulate SNO and other NO metabolite profile of murine blood and liver tissue. Since there is no information to date on the effect of multiple meningococcal denitrification genes (aniA and norB) on the cellular pathology of meningococcal sepsis, we constructed and characterised a combination of NO metabolising gene mutants (ΔaniA/ΔnorB, ΔnsrR/ΔnorB, ΔaniA/ΔnorB/ΔnsrR) using the isocloning method. Differentiated human primary bronchial airway epithelial cells cultured at an air-liquid interface (HPEC-ALI) are polarised cells with tight junctions, possessing similar characteristics to the nasopharyngeal epithelial cells with which meningococci have to interact during colonisation and pathogenesis. HPEC-ALIs were infected with the newly created mutants (ΔaniA/ΔnorB and ΔaniA/ΔnorB/ΔnsrR) to examine the role of bacterial NO metabolism on the barrier function and immune response, functions known to be modulated by high concentrations of NO present in the airway epithelium. We demonstrated bacterial burden inversely correlates with the barrier function (TER) but positively with the cytokine profile (IL-8, TNFα). However, meningococcal denitrification does not have any differential role in the regulation of barrier function and cytokine profile of the HPEC-ALIs in the experimental system we used. The role of meningococcal denitrification in biofilm formation in vitro was also investigated. Preliminary data showed when biofilm formation was induced by nutrient starvation, ΔaniA/ΔnorB showed a significantly reduced biofilm forming ability compared to the Wt strain measured by the crystal violet staining. To investigate the role of aniA in differential regulation of biofilm formation, reverse complemented strains (ΔaniA/aniAIPTG+ and ΔaniA/aniA+) were created. Characterisation data showed functional activation was restored in ΔaniA when aniA was complemented along with the upstream regulatory elements such as the endogenous promoter (ΔaniA/aniA+) but not when aniA coding region was complemented under the control of an IPTG inducible lac promoter (ΔaniA/aniAIPTG+).
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Cordes, Frank Stephan. "Biophysical studies of bacterial pathogenesis." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404113.

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Borodina, Elena. "Bacterial metabolism of dimethylsulfone." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251998.

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Green, Luke Richard. "The role of teraspanins in bacterial pathogenesis." Thesis, University of Sheffield, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522436.

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Kaittanis, Charalambos. "Magnetic nanosensors for multiplexed bacterial pathogenesis identification." Doctoral diss., University of Central Florida, 2010. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4610.

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Developing diagnostic modalities that utilize nanomaterials and miniaturized detectors can have an impact in point-of-care diagnostics. Diagnostic systems that (i) are sensitive, robust, and portable, (ii) allow detection in clinical samples, (iii) require minimal sample preparation yielding results quickly, and (iv) can simultaneously quantify multiple targets, would have a great potential in biomedical research and public healthcare. Bacterial infections still cause pathogenesis throughout the world (Chapter I). The emergence of multi-drug resistant strains, the potential appearance of bacterial pandemics, the increased occurrence of bacterial nosocomial infections, the wide-scale food poisoning incidents and the use of bacteria in biowarfare highlight the need for designing novel bacterial-sensing modalities. Among the most prominent disease-causing bacteria are strains of Escherichia coli, like the E. coli O157:H7 that produces the Shiga-like toxin (Stx). Apart from diarrheagenic E. coli strains, others cause disease varying from hemolytic uremic syndrome and urinary tract infections to septicemia and meningitis. Therefore, the detection of E. coli needs to be performed fast and reliably in diverse environmental and clinical samples. Similarly, Mycobacterium avium spp. paratuberculosis (MAP), a fastidious microorganism that causes Johne's disease in cattle and has been implicated in Crohn's disease (CD) etiology, is found in products from infected animals and clinical samples from CD patients, making MAP an excellent proof-of-principle model. Recently, magnetic relaxation nanosensors (MRnS) provided the first applications of improved diagnostics with high sensitivity and specificity.; Furthermore, these MRnS achieved equally fast IS900 detection even in crude DNA extracts, outperforming the gold standard diagnostic method of nested Polymerase Chain Reaction (nPCR). Likewise, the MRnS detected IS900 with unprecedented sensitivity and specificity in clinical isolates obtained from blood and biopsies of CD patients, indicating the clinical utility of these nanosensors. Subsequently, we designed MRnS for the detection of MAP via surface-marker recognition in complex matrices (Chapter III). Milk and blood samples containing various concentrations of MAP were screened and quantified without any processing via MRnS, obtaining dynamic concentration-dependent curves within an hour. The MAP MRnS were able not only to identify their target in the presence of interferences from other Gram positive and Gram negative bacteria, but could differentiate MAP among other mycobacteria including Mycobacterium tuberculosis. In addition, detection of MAP was performed in clinical isolates from CD patients and homogenized tissues from Johne's disease cattle, demonstrating for the first time the rapid identification of bacteria in produce, as well as clinical and environmental samples. However, comparing the unique MAP quantification patterns with literature-available trends of other targets, we were prompted to elucidate the underlying mechanism of this novel behavior (Chapter IV). We hypothesized that the nanoparticle valency--the amount of probe on the surface of the MRnS --may have modulated the changes in the relaxation times (delta]T2) upon MRnS--target association. To address this, we prepared MAP MRnS with high and low anti-MAP antibody levels using the same nanoparticle formulation. Results corroborated our hypothesis, but to further bolster it we investigated if this behavior is target-size-independent.; Hence utilizing small-molecule- and antibody-carrying MRnS, we detected cancer cells in blood, observing similar detection patterns that resembled those of the bacterial studies. Notably, a single cancer cell was identified via high-valency small-molecule MRnS, having grave importance in cancer diagnostics because a single cancer cell progenitor in circulation can effectively initiate the metastatic process. Apart from cells, we also detected the Cholera Toxin B subunit with valencly-engineered MRnS, observing similar to the cellular targets' diagnostic profiling behavior. Finally, as bacterial drug resistance is of grave healthcare importance, we utilized MRnS for the assessment of bacterial metabolism and drug susceptibility (Chapter V). Contrary to spectophotometric and visual nanosensors, their magnetic counterparts were able to quickly assess bacterial carbohydrate uptake and sensitivity to antibiotics even in blood. Two MRnS-based assay formats were devised relying on either the Concanavalin A (Con A)-induced clustering of polysaccharide-coated nanoparticles or the association between free carbohydrates and Con A-carrying MRnS. Overall, taking together these results, as well as those on pathogen detection and the recent instrumentation advancements, the use of MRnS in the clinic, the lab and the field should be anticipated.; Nucleic acids, proteins, viruses and enzymatic activity were probed, yet neither large targets (for instance bacterial and mammalian cells) nor multiple bacterial disease parameters have been simultaneously monitored, in order to provide thorough information for clinical decision making. Therefore, the goal of this study was to utilize MRnS for the sensitive identification of multiple targets associated with bacterial pathogenesis, while monitoring virulence factors at the microorganism, nucleic acid and virulence factor levels, to facilitate improved diagnosis and optimal treatment regimes. To demonstrate the versatility of MRnS, we used MAP as our model system, as well as several other pathogens and eukaryotic cell lines. In initial studies, we developed MRnS suitable for biomedical applications (Chapter II). The resulting MRnS were composed of an iron oxide core, which was caged within a biodegradable polymeric coating that could be further functionalized for the attachment of molecular probes. We demonstrated that depending on the polymer used the physical and chemical properties of the MRnS can be tailored. Furthermore, we investigated the role of polymer in the enzyme-mimicking activity of MRnS, which may lead to the development of optimized colorimetric in vitro diagnostic systems such as immunoassays and small-molecule-based screening platforms. Additionally, via facile conjugation chemistries, we prepared bacterium-specific MRnS for the detection of nucleic acid signatures (Chapter III). Considering that MAP DNA can be detected in clinical samples and isolates from CD patients via laborious isolation and amplification procedures requiring several days, MRnS detected MAP's IS900 nucleic acid marker up to a single MAP genome copy detection within 30 minutes.
ID: 028916614; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Thesis (Ph.D.)--University of Central Florida, 2010.; Includes bibliographical references (p. 139-150).
Ph.D.
Doctorate
Burnett School of Biomedical Sciences
Medicine
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Vdovikova, Svitlana. "Roles of membrane vesicles in bacterial pathogenesis." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-138714.

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The production of membranous vesicles is observed to occur among organisms from all domains of the tree of life spanning prokaryotes (bacteria, archaea) and eukaryotes (plants, animals and fungi). Bacterial release of membrane-derived vesicles (MVs) has been studied most extensively in cases of Gram-negative species and implicating their outer membrane in formation of extracellular MVs. However, recent studies focusing on Gram-positive bacteria have established that they also undergo MV formation. Membrane vesicles are released during normal bacterial growth, they are derived from the bacterial membrane(s) and may function as transporters of different proteins, DNA and RNA to the neighbouring bacteria or to the cells of a mammalian host. The transport of virulence factors in a condensed manner via MVs to the host cells presumably protects these proteins from degradation and, thereby, targets the host cells in a specific manner. The aim of my thesis is to investigate secretion of MV-associated virulence factors and to study interactions of MVs produced by two selected Gram-negative and Gram-positive bacteria, i.e. Vibrio cholerae and Listeria monocytogenes, with eukaryotic host cells. Depending on whether the bacterium acts as an extracellular or intracellular pathogen, MVs may be considered to have specific functions, which may lead to the different outcomes of MV-host interactions. V. cholerae transport systems for virulence factors include the Type VI secretion system and MVs (also referred to as the “Type 0” secretion system). We have identified that the biologically active form of PrtV protease in different V. cholerae serogroups is transported via MVs. PrtV protease is essential for V. cholerae environmental survival and protection from natural predator grazing. We demonstrated that PrtV is primarily translocated via the inner membrane to the periplasmic space, where it undergoes autoproteolysis, and the truncated version of PrtV protein is packaged inside the MVs and released from the surface of bacteria. MV-associated PrtV protease showed a contribution to bacterial resistance towards the antimicrobial peptide LL-37, thereby, enhancing bacterial survival by avoiding this innate immune defense of the host. We also studied another virulence factor of V. cholerae, the pore-forming toxin VCC, which was found to be transported by MVs. MV-associated VCC is biologically active and triggers an autophagic response in the target cells. We suggested that autophagy serves as a cellular defense mechanism against the MV-associated bacterial virulence factor of V. cholerae. Listeria monocytogenes is a Gram-positive intracellular and facultative anaerobic food-borne pathogen causing listeriosis. It causes only sporadic outbreaks in healthy individuals, however, it is dangerous for a fetus or newborn child, and for pregnant and immunocompromised people, leading to a deadly infection in one third of the cases. We have analyzed MVs produced by L. monocytogenes and their interaction with eukaryotic cells. Confocal microscopy analysis showed that MVs are internalized into HeLa and HEK293 cells and are accumulated in lysosomes. Moreover, L. monocytogenes produces MVs inside the host cells and even inside the phagosomes. We found that the major virulence factor of L. monocytogenes, the cholesterol-dependent pore-forming protein listeriolysin O (LLO), is entrapped inside the MVs and resides there in an oxidized inactive state. LLO is known to induce autophagy by making pores in the phagosomal membrane of targeted eukaryotic cells. In our studies, we have shown that MVs effectively abrogated autophagy induced by Torin1, by purified LLO or by another pore-forming toxin from V. cholerae. We also found that MVs promote bacterial intracellular survival inside mouse embryonic fibroblasts. In addition, MVs have been shown to have a strong protective activity against host cell necrosis initiated by pore-forming toxin. Taken together, these findings suggested that in vivo MVs production from L. monocytogenes might be a relevant strategy of bacteria to manipulate host responses and to promote bacterial survival inside the host cells.
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Woods, Nigel R. "The bacterial metabolism of propane." Thesis, University of Warwick, 1988. http://wrap.warwick.ac.uk/98056/.

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A range of enrichment/isolation procedures yielded over 80 strains of Gram-positive propane-utilizing bacteria from a variety of environments. All appeared to be members of the Corynebacterium-Mycobacterium-Nocardia complex. No Gram-negative organisms were isolated and screening of Pseudomonas spp. culture collections failed to isolate any gaseous alkane-utilizing strains. Three of the isolated strains, identified as Rhodococcus rhodochrous. R. erythropolis and a Mycobacterium sp., were subjected to further analyses. They showed differing specificities towards gaseous alkane substrates, R. rhodochrous growing only on propane, the Mycobacterium sp. on ethane and propane, and R. erythropolis on all three. None could grow on alkenes but all could epoxidate propene to 1,2-epoxypropane after growth on propane. R. rhodochrous (designated strain PNKbl) was selected for detailed study. Its potential to epoxidate alkenes was investigated further. Attempts to grow the organism in steady-state, continuous culture on propane were unsuccessful. It grew batchwise on most of the putative Intermediates of propane metabolism. Simultaneous adaptation studies using whole cells suggested that the organism had the potential to use either the terminal or subterminal pathways of propane metabolism. SDS-polyacrylamide gel electrophoresis revealed proteins of molecular weight 67, 59, 57 kDal specific to cells grown on propane, which may be components of the propane-oxidizing system. Oxygenase activity induced by propane, was studied in whole cell and cell-free systems and results suggest that it may be different in nature to those previously described alkane oxygenase systems. The enzyme complement of propane-grown cells suggested that propane could be assimilated by either terminal or subterminal oxidation pathways and the relative importance of each remains unclear.
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Erdlenbruch, Barbara Nicole Susanne. "Bacterial metabolism of short chain alkanesulfonates." Thesis, University of Warwick, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250990.

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de, Klerk Nele. "Host-bacteria interactions : Host cell responses and bacterial pathogenesis." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-126425.

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Helicobacter pylori colonizes the human stomach, where it causes gastritis that may develop into peptic ulcer disease or cancer when left untreated. Neisseria gonorrhoeae colonizes the urogenital tract and causes the sexually transmitted disease gonorrhea. In contrast, Lactobacillus species are part of the human microbiota, which is the resident microbial community, and are considered to be beneficial for health. The first host cell types that bacteria encounter when they enter the body are epithelial cells, which form the border between the inside and the outside, and macrophages, which are immune cells that engulf unwanted material.       The focus of this thesis has been the interaction between the host and bacteria, aiming to increase our knowledge of the molecular mechanisms that underlie the host responses and their effects on bacterial pathogenicity. Understanding the interactions between bacteria and the host will hopefully enable the development of new strategies for the treatment of infectious disease. In paper I, we investigated the effect of N. gonorrhoeae on the growth factor amphiregulin in cervical epithelial cells and found that the processing and release of amphiregulin changes upon infection. In paper II, we examined the expression of the transcription factor early growth response-1 (EGR1) in epithelial cells during bacterial colonization. We demonstrated that EGR1 is rapidly upregulated by many different bacteria. This upregulation is independent of the pathogenicity, Gram-staining type and level of adherence of the bacteria, but generally requires viable bacteria and contact with the host cell. The induction of EGR1 is mediated primarily by signaling through EGFR, ERK1/2 and β1-integrins. In paper III, we described the interactions of the uncharacterized protein JHP0290, which is secreted by H. pylori, with host cells. JHP0290 is able to bind to several cell types and induces apoptosis and TNF release in macrophages. For both of these responses, signaling through Src family kinases and ERK is essential. Apoptosis is partially mediated by TNF release. Finally, in paper IV, we showed that certain Lactobacillus strains can reduce the colonization of H. pylori on gastric epithelial cells. Lactobacilli decrease the gene expression of SabA and thereby inhibit the binding mediated by this adhesin.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Manuscript. Paper 4: Manuscript.

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Gonçalves, Carla Aguiar. "The role of polyunsaturated fatty acids in bacterial pathogenesis." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13794.

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Mestrado em Biotecnologia
Polyunsaturated fatty acids (PUFAs) comprise a class of essential micronutrients, which are essential for normal development, cardiovascular health, and immunity. The role of lipids, including long-chain fatty acids, in the immune response is increasingly being recognized as beneficial regulators of the immune systems. However, the mechanisms by which PUFAs modulate innate immunity are yet to be fully clarified. C. elegans has been used in several recent studies as a simple animal model for the study of host-pathogen interactions, generating important insights into both bacterial pathogenesis and host innate immunity. Many of the virulence mechanisms used by bacterial pathogens to cause disease in mammalian hosts have also been shown to be important for pathogenesis in C. elegans and, similarly, important features of the host innate immunity have been evolutionarily conserved between C. elegans and mammals. This project is focused on addressing the role of polyunsaturated fatty acids in bacterial pathogenesis using C. elegans as model system. We find that knockdown of some elongase genes increase the worms’ susceptibility towards infection with the adherent-invasive Escherichia Coli LF82, isolated from a patient suffering from Crohn’s disease. Moreover, dietary supplementation with the fatty acid γ-linolenic acid rescued the enhanced pathogen susceptibility of C. elegans lacking a Δ6 desaturase. The fatty acid profile of the nematode is altered upon infection with pathogenic LF82. qRT-PCR analysis allowed to determine that stress and autophagy genes are induced in C. elegans infected with this particular type of E. coli. Autophagy was found to be increased on C. elegans challenged with LF82, as determined by fluorescence microscopy. Collectively these results suggest an important role for PUFAS in the innate immune response and indicate that autophagy may have a contribution for C. elegans response towards the pathogen E. coli LF82.
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Books on the topic "Bacterial metabolism and pathogenesis"

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Metabolism and bacterial pathogenesis. Washington, DC: ASM Press, 2015.

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1932-, Levin Jack, and International Endotoxin Society Congress, eds. Endotoxin and sepsis: Molecular mechanisms of pathogenesis, host resistance, and therapy. New York: Wiley-Liss, 1998.

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E, Faist, and Merck Sharp & Dohme., eds. Differential release and impact of antibiotic-induced endotoxin. New York: Raven Press, 1995.

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Nordenfelt, Pontus, and Mattias Collin, eds. Bacterial Pathogenesis. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6673-8.

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DeLeo, Frank R., and Michael Otto, eds. Bacterial Pathogenesis. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-032-8.

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1945-, Clark Virginia L., and Bavoil Patrik M, eds. Bacterial pathogenesis. San Diego: Academic Press, 1994.

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Nordenfelt, Pontus, and Mattias Collin, eds. Bacterial Pathogenesis. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3243-7.

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Gottschalk, Gerhard. Bacterial Metabolism. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-1072-6.

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Bacterial metabolism. 2nd ed. New York: Springer-Verlag, 1986.

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1929-, Köhler Werner, Pulverer Gerhard, and Przondo-Mordarska Anna, eds. Bacterial pathogenesis: Modern approaches. Halle: Deutsche Akademie der Naturforscher Leopoldina, 1999.

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Book chapters on the topic "Bacterial metabolism and pathogenesis"

1

Wolfe, Alan J. "Glycolysis for the Microbiome Generation." In Metabolism and Bacterial Pathogenesis, 1–16. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch1.

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Alteri, Christopher J., and Harry L. T. Mobley. "Metabolism and Fitness of Urinary Tract Pathogens." In Metabolism and Bacterial Pathogenesis, 215–30. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch10.

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Armstrong, Sandra K. "Bacterial Metabolism in the Host Environment: Pathogen Growth and Nutrient Assimilation in the Mammalian Upper Respiratory Tract." In Metabolism and Bacterial Pathogenesis, 231–61. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch11.

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Jakubovics, Nicholas S. "Saliva as the Sole Nutritional Source in the Development of Multispecies Communities in Dental Plaque." In Metabolism and Bacterial Pathogenesis, 263–77. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch12.

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Pacheco, Alline R., and Vanessa Sperandio. "Enteric Pathogens Exploit the Microbiota-generated Nutritional Environment of the Gut." In Metabolism and Bacterial Pathogenesis, 279–96. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch13.

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Stecher, Bärbel. "The Roles of Inflammation, Nutrient Availability and the Commensal Microbiota in Enteric Pathogen Infection." In Metabolism and Bacterial Pathogenesis, 297–320. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch14.

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Haines-Menges, Brandy L., W. Brian Whitaker, J. B. Lubin, and E. Fidelma Boyd. "Host Sialic Acids: A Delicacy for the Pathogen with Discerning Taste." In Metabolism and Bacterial Pathogenesis, 321–42. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch15.

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Conway, Tyrrell, and Paul S. Cohen. "Commensal and Pathogenic Escherichia coli Metabolism in the Gut." In Metabolism and Bacterial Pathogenesis, 343–62. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch16.

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Nataro, James P. "Pathogenesis - Thoughts from the Front Line." In Metabolism and Bacterial Pathogenesis, 17–26. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch2.

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Eisenreich, Wolfgang, Jürgen Heesemann, Thomas Rudel, and Werner Goebel. "Metabolic Adaptations of Intracellullar Bacterial Pathogens and their Mammalian Host Cells during Infection (“Pathometabolism”)." In Metabolism and Bacterial Pathogenesis, 27–58. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818883.ch3.

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Conference papers on the topic "Bacterial metabolism and pathogenesis"

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Al-Asmar, Jawaher, Sara Rashwan, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Bacterial Infection on Host Survival and Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0186.

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Enterobacteriaceae, a large family of facultative anaerobic bacteria, encloses a broad spectrum of bacterial species including Escherichia coli, Salmonella enterica, and Shigella sonnei, that produce enterotoxins and cause gastrointestinal tract diseases. While much is known about the regulation and function of enterotoxins within the intestine of the host; the lack of cheap, practical, and genetically tractable model organisms has restricted the investigation of others facets of this host-pathogen interaction. Our group, among others, has employed Drosophila melanogaster, as a model organism to shed more light on some aspects of host-pathogen interplays. In this project, we addressed the effect of Escherichia coli, Salmonella enterica, and Shigella sonnei infection on altering the metabolic homeostasis of the host. Drosophila melanogaster flies were orally infected with Escherichia coli, Salmonella enterica, or Shigella sonnei, a method that mimics the natural route used by enteric pathogens to gain access to the gastrointestinal tract in humans. The results of our study revealed that both Escherichia coli and Shigella sonnei pathogens were capable of colonizing the host gut, resulting in a reduction in the life span of the infected host. Escherichia coli and Shigella sonnei infected flies also exhibited altered metabolic profiles including lipid droplets deprivation from their fat body (normal lipid storage organ in flies), irregular accumulation of lipid droplets in their gut, and significant elevation of systemic glucose and triglyceride levels. These metabolic alterations could be mechanistically attributed to the differential down-regulation in the expression of metabolic peptide hormones (Allatostatin A, Diuretic hormone 31, and Tachykinin) detected in the gut of Escherichia coli and Shigella sonnei infected flies. Salmonella enterica; however, was unable to colonize the gut of the host; and therefore, Salmonella enterica infected flies exhibited a relatively normal metabolic status as that of non infected flies. Gaining a proper mechanistic understanding of infection-induced metabolic alterations helps in modulating the pathogenesis of gastrointestinal tract diseases in a host and opens up for promising therapeutic approaches for infection induced metabolic disorders
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Ji, Xiangming Ji, Jun Qian, Jamshedur Rahman, Brad Harris, Megan Hoeksema, Heidi Chen, Rosana Eisenberg, and Jamey Young. "Abstract A10: SLC7A11 contributes to the pathogenesis of lung cancer." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a10.

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Egorova, Elena V., Tatyana M. Manikovskaya, and Yury K. Shapovalov. "The role of aminothiolis in the pathogenesis of chronic rhinosinusitis of bacterial etiology." In Актуальные вопросы оториноларингологии. Благовещенск: Амурская государственная медицинская академия, 2022. http://dx.doi.org/10.22448/9785604863312_48.

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Lebedeva, Olga. "PATTERN-RECOGNITION RECEPTORS, ACTIVATED BY BACTERIAL LIGANDS, IN PATHOGENESIS OF MISSED AND SPONTANEOUS ABORTIONS." In 4th SGEM International Multidisciplinary Scientific Conferences on SOCIAL SCIENCES and ARTS Proceedings. STEF92 Technology, 2017. http://dx.doi.org/10.5593/sgemsocial2017/33/s12.059.

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Chu, Dominique. "Replaying the tape of evolution: Evolving parameters for a simple bacterial metabolism." In 2013 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2013. http://dx.doi.org/10.1109/cec.2013.6557573.

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Taylor, Holly, Jaroslav Slamecka, Alla Musiyenko, Elaine Gavin, Tiffany S. Norton, Ileana Aragon, Taylor Young, et al. "Abstract B31: Tumor-intrinsic B7-H3 regulates drug resistance, metabolism, and pathogenesis in ovarian cancer." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-b31.

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PHILPOTT, DANA J., JONATHAN D. EDGEWORTH, and PHILIPPE J. SANSONETTI. "THE PATHOGENESIS OF SHIGELLA FLEXNERI INFECTION: LESSONS FROM IN VITRO AND IN VIVO STUDIES." In The Activities of Bacterial Pathogens in Vivo - Based on Contributions to a Royal Society Discussion Meeting. IMPERIAL COLLEGE PRESS, 2001. http://dx.doi.org/10.1142/9781848161610_0003.

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HEITHOFF, DOUGLAS M., ROBERT L. SINSHEIMER, DAVID A. LOW, and MICHAEL J. MAHAN. "IN VIVO GENE EXPRESSION AND THE ADAPTIVE RESPONSE: FROM PATHOGENESIS TO VACCINES AND ANTIMICROBIALS." In The Activities of Bacterial Pathogens in Vivo - Based on Contributions to a Royal Society Discussion Meeting. IMPERIAL COLLEGE PRESS, 2001. http://dx.doi.org/10.1142/9781848161610_0008.

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Terres, W., C. Hamm, W. Kupper, and W. Bleifeld. "PLATELET AGGREGABLLITY AND METABOLISM IN PATIENTS WITH UNSTABLE ANGINA PECTORIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643777.

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Several platelet products indicating platelet activation have been detected in blood and urine of patients (PTS) with angina pectoris (AP) at rest. Platelet activation mainly depends on local changes in the morphology or biochemical behaviour of the vessels. Whether platelet hyperaggregability is of additional importance in the pathogenesis of unstable AP is up to now unclear. In a prospective trial we therefore evaluated 32 patients (PTS) with coronary heart disease, 16 with AP at rest during the last 8 hours before blood collection and 16 age and sex matched controls with stable exertional AP. Platelet aggregation was measured upon stimulation with ADP (0.5, 1 and 10 μmol/l) and collagen (1and 5μg/ml), and c-AMP was determined in platelet rich plasma before, and, as an estimate of platelet adenylate cyclase activity, after stimulation of this enzyme with PGE 1 (10 μmol/l for 30 s). For all concentrations of both ADP and collagen no significant differences in the rates and extents of aggregation could be found between the groups. Correspondingly, the mean (±. 2 SEM) concentrations of c-AMP were similar, basally (4.1 ±.1.4 pmol/ml for PTS withunstable AP and 5.3 t 1.3 pmol/ml for PTS with stable AP)and after stimulation of platelet adenylate cyclase with PGE 1 (14.8 ± 4.1 vs. 17.2 ± 2.8 pmol/ml).Conclusion: No generalized platelet hyperaggregability could be detected in our PTS with unstable AP when compared to controls with stable exertional AP.
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Yarkova, V. G., V. A. Zhmurov, and E. B. Klester. "THE ROLE OF MAGNESIUM DEFICIENCY IN THE PATHOGENESIS OF THE FORMATION OF ARTERIAL HYPERTENSION IN WORKERS OF LOCOMOTIVE CREWS. CORRECTION METHODS." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-607-611.

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Abstract: Purpose of the study: To assess the effects of magnesium deficiency on the indices of lipid metabolism in patients with an arterial hypertension locomotive crews. Purpose of the work: To assess the effect of magnesium deficiency on the pathogenesis of the formation of arterial hypertension in workers of locomotive crews. Correction methods. Materials and methods: This work presents an analysis of the results of clinical observation, special biochemical and functional studies of 136 male patients with arterial hypertension, workers of locomotive crews. Results: In workers of locomotive crews patients with hypertension, increased individual cardiovascular risk according to the SCORE scale, remodeling of the cardiovascular system, as well as the risk of developing occupational disability are interrelated with signs of magnesium deficiency. Conclusion: The inclusion of a complex preparation of magnesium and vitamin B6 in the therapy of arterial hypertension in workers of locomotive crews has a significant effect on the clinical manifestations of chronic stress, magnesium deficiency, improves the dynamics of lipid metabolism, the structural and functional state of the cardiovascular system, and professionally important qualities.
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Reports on the topic "Bacterial metabolism and pathogenesis"

1

NEALSON, H. K. GROWTH AND METABOLISM OF INDIVIDUAL BACTERIAL CELLS UTILIZING NANOSIMS. Office of Scientific and Technical Information (OSTI), August 2007. http://dx.doi.org/10.2172/1034346.

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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

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Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.
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Segelke, B. 19-LW-045 Full Length Final Report. Molecular Mechanisms of Bacterial Pathogenesis: Waging the Arms Race with Superbugs. Office of Scientific and Technical Information (OSTI), January 2021. http://dx.doi.org/10.2172/1756727.

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Maier, Robert J. Bacterial nickel metabolism and storage. Final report for the period January 1, 1999 - March 31, 2002. Office of Scientific and Technical Information (OSTI), August 2002. http://dx.doi.org/10.2172/804171.

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Maier, Robert J. Bacterial nickel metabolism and storage. Final technical report for period January 1, 1994 - August 31, 1998. Office of Scientific and Technical Information (OSTI), March 2001. http://dx.doi.org/10.2172/808345.

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Cohen, Jerry D., and Ephraim Epstein. Metabolism of Auxins during Fruit Development and Ripening. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7573064.bard.

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We had proposed to look at several aspects of auxin metabolism in fruit tissues: 1) IAA biosynthesis from tryptophan and IAA biosynthesis via the non-tryptophan pathway; 2) changes in the capacity to form conjugates and catabolites of auxin at different times during fruit development and; 3) the effects of modifying auxin metabolism in fruit tissues. The latter work focused primarily on the maize iaglu gene, with initial studies also using a bacterial gene for hydrolysis of IAA-aspartate. These metabolic and molecular studies were necessary to define potential benefits of auxin metabolism modification and will direct future efforts for crop improvement by genetic methods. An in vitro system was developed for the production of tomato fruit in culture starting from immature flowers in order to ascertain the effect of auxin modification on fruit ripening. IAA supplied to the fruit culture media prior to breaker stage resulted in an increase in the time period between breaker and red-ripe stages from 7 days without additional IAA to 12 days when 10-5 M IAA was added. These results suggest that significant changes in the ripening period could be obtained by alteration of auxin relationships in tomato fruit. We generated transgenic tomato plants that express either the maize iaglu gene or reduced levels of the gene that encodes the enzyme IAA-glucose synthetase. A modified shuttle vector pBI 121 expressing the maize iaglu gene in both sense and antisense orientations under a 35S promoter was used for the study. The sense plants showed total lack of root initiation and development. The antisense transgenic plants, on the other hand, had unusually well developed root systems at early stages in development. Analysis showed that the amount and activity of the endogenous 75 kDa IAGLU protein was reduced in these plants and consequently these plants had reduced levels of IAA-glucose and lower overall esterified IAA.
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Gutnick, David, and David L. Coplin. Role of Exopolysaccharides in the Survival and Pathogenesis of the Fire Blight Bacterium, Erwinia amylovora. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568788.bard.

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Fireblight, a disease of apples and pears, is caused by Erwinia amylovora. Mutants of E. amylovora that do not produce the extreacellular polysaccharide (EPS), amylovoran, are avirulent. A similar EPS, stewartan, is produced by E. stewartii, which caused Stewart's wilt of corn, and which has also been implicated in the virulence of this strain. Both stewartan and amylovoran are type 1 capsular polysaccharides, typified by the colanic acid slime produced by Escherichia coli. Extracellular polysaccharide slime and capsules are important for the virulence of bacterial pathogens of plants and animals and to enhance their survival and dissemination outside of the host. The goals of this project were to examine the importance of polysaccharide structure on the pathogenicity and survival properties of three pathogenic bacteria: Erwinia amylovora, Erwinia stewartii and Escherichia coli. The project was a collaboration between the laboratories of Dr. Gutnick (PI, E. coli genetics and biochemistry), Dr. Coplin (co-PI, E. stewartii genetics) and Dr. Geider (unfunded collaborator, E. amylovora genetics and EPS analysis). Structural analysis of the EPSs, sequence analysis of the biosynthetic gene clusters and site-directed mutagenesis of individual cps and ams genes revealed that the three gene clusters shared common features for polysaccharide polymerization, translocation, and precursor synthesis as well as in the modes of transcriptional regulation. Early EPS production resulted in decreased virulence, indicating that EPS, although required for pathogenicity, is anot always advantageous and pathogens must regulate its production carefully.
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Alfano, James, Isaac Barash, Thomas Clemente, Paul E. Staswick, Guido Sessa, and Shulamit Manulis. Elucidating the Functions of Type III Effectors from Necrogenic and Tumorigenic Bacterial Pathogens. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592638.bard.

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Many phytopathogenic bacteria use a type III protein secretion system (T3SS) to inject type III effectors into plant cells. In the experiments supported by this one-year feasibility study we investigated type III effector function in plants by using two contrasting bacterial pathogens: Pseudomonas syringae pv. tomato, a necrotrophic pathogen and Pantoea agglomerans, a tumorigenic pathogen. The objectives are listed below along with our major conclusions, achievements, and implications for science and agriculture. Objective 1: Compare Pseudomonas syringae and Pantoea agglomerans type III effectors in established assays to test the extent that they can suppress innate immunity and incite tumorigenesis. We tested P. agglomerans type III effectors in several innate immunity suppression assays and in several instances these effectors were capable of suppressing plant immunity, outputs that are suppressed by P. syringae effectors. Interestingly, several P. syringae effectors were able to complement gall production to a P. agglomerans pthGmutant. These results suggest that even though the disease symptoms of these pathogens are dramatically different, their type III effectors may function similarly. Objective 2: Construct P. syringae mutants in different combinations of type III-related DNA clusters to reduce type III effector redundancy. To determine their involvement in pathogenicity we constructed mutants that lack individual and multiple type III-related DNA clusters using a Flprecombinase-mediated mutagenesis strategy. The majority of single effector mutants in DC3000 have weak pathogenicity phenotypes most likely due to functional redundancy of effectors. Supporting this idea, Poly-DNAcluster deletion mutants were more significantly reduced in their ability to cause disease. Because these mutants have less functional redundancy of type III effectors, they should help identify P. syringae and P. agglomerans effectors that contribute more significantly to virulence. Objective 3: Determine the extent that P. syringae and P. agglomerans type III effectors alter hormone levels in plants. Inhibition of auxin polar transport by 2,3,5-triiodobenzoic acid (TIBA) completely prevented gall formation by P. agglomerans pv. gypsophilae in gypsophila cuttings. This result supported the hypothesis that auxin and presumably cytokinins of plant origin, rather than the IAA and cytokinins secreted by the pathogen, are mandatory for gall formation. Transgenic tobacco with pthGshowed various phenotypic traits that suggest manipulation of auxin metabolism. Moreover, the auxin levels in pthGtransgenic tobacco lines was 2-4 times higher than the control plants. External addition of auxin or cytokinins could modify the gall size in gypsophila cuttings inoculated with pthGmutant (PagMx27), but not with other type III effectors. We are currently determining hormone levels in transgenic plants expressing different type III effectors. Objective 4: Determine whether the P. agglomerans effectors HsvG/B act as transcriptional activators in plants. The P. agglomerans type III effectors HsvG and HsvB localize to the nucleus of host and nonhost plants and act as transcription activators in yeast. Three sites of adjacent arginine and lysine in HsvG and HsvB were suspected to act as Nuclear localization signals (NLS) domains. A nuclear import assay indicated two of the three putative NLS domains were functional NLSs in yeast. These were shown to be active in plants by fusing HsvG and HsvB to YFP. localization to the nucleus was dependent on these NLS domains. These achievements indicate that our research plan is feasible and suggest that type III effectors suppress innate immunity and modulate plant hormones. This information has the potential to be exploited to improve disease resistance in agricultural crops.
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Zhao, Bingyu, Saul Burdman, Ronald Walcott, and Gregory E. Welbaum. Control of Bacterial Fruit Blotch of Cucurbits Using the Maize Non-Host Disease Resistance Gene Rxo1. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699843.bard.

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The specific objectives of this BARD proposal were: (1) To determine whether Rxol can recognize AacavrRxo1 to trigger BFB disease resistance in stable transgenic watermelon plants. (2) To determine the distribution of Aac-avrRxo1 in a global population of Aae and to characterize the biological function of Aac-avrRxo1. (3) To characterize other TIS effectors of Aae and to identify plant R gene(s) that can recognize conserved TIS effectors of this pathogen. Background to the topic: Bacterial fruit blotch (BFB) of cucurbits, caused by Acidovorax avenae subsp. citrulli (Aae), is a devastating disease that affects watermelon (Citrullus lanatus) and melon (Cucumis melo) production worldwide, including both Israel and USA. Two major groups of Aae strains have been classified based on their virulence on host plants, genetics and biochemical properties. Thus far, no effective resistance genes have been identified from cucurbit germplasm. In this project, we assessed the applicability of a non-host disease resistance gene, Rxol, to control BFB in watermelon. We also tried to identify Aae type III secreted (TIS) effectors that can be used as molecular probes to identify novel disease resistance genes in both cucurbits and Nieotianatabaeum. Major conclusions, solutions, achievements: We generated five independent transgenic watermelon (cv. Sugar Babay) plants expressing the Rxol gene. The transgenic plants were evaluated with Aae strains AAC001 and M6 under growth chamber conditions. All transgenic plants were found to be susceptible to both Aae strains. It is possible that watermelon is missing other signaling components that are required for Rxol-mediated disease resistance. In order to screen for novel BFB resistance genes, we inoculated two Aae strains on 60 Nieotiana species. Our disease assay revealed Nicotiana tabaeum is completely resistant to Aae, while its wild relative N. benthamiana is susceptible to Aae. We further demonstrated that Nieotiana benthamiana can be used as a surrogate host for studying the mechanisms of pathogenesis of Aae. We cloned 11 TIS effector genes including the avrRxolhomologues from the genomes of 22 Aae strains collected worldwide. Sequencing analysis revealed that functional avrRxol is conserved in group" but not group I Aae strains. Three effector genes- Aave_1548, Aave_2166 and Aave_2708- possessed the ability to trigger an HR response in N. tabacum when they were transiently expressed by Agrobaeterium. We conclude that N. tabacum carries at least three different non-host resistance genes that can specifically recognize AaeTIS effectors to trigger non-host resistance. Screening 522 cucurbits genotypes with two Aae strains led us to identify two germplasm (P1536473 and P1273650) that are partially resistant to Aae. Interestingly, transient expression of the TIS effector, Aave_1548, in the two germplasms also triggered HR-Iike cell death, which suggests the two lines may carry disease resistance genes that can recognize Aave_1548. Importantly, we also demonstrated that this effector contributes to the virulence of the bacterium in susceptible plants. Therefore, R genes that recognize effector Aave1548 have great potential for breeding for BFB resistance. To better understand the genome diversity of Aae strains, we generated a draft genome sequence of the Israeli Aae strain, M6 (Group I) using Iliumina technology. Comparative analysis of whole genomes of AAC001, and M6 allowed us to identify several effectors genes that differentiate groups I and II. Implications, both scientific and agricultural: The diversity of TIS effectors in group I and II strains of Aae suggests that a subset of effectors could contribute to the host range of group I and II Aae strains. Analysis of these key effectors in a larger Aae population may allow us to predict which cucurbit hosts may be at risk to BFB. Additionally, isolation of tobacco and cucurbit Rgenes that can recognize Aae type III effectors may offer new genetic resources for controlling BFB.
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10

Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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