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Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Campylobacter spp. readily colonize the intestinal tracts of both human and avian species. While most often commensal organisms in birds, campylobacters remain the leading cause of bacterial gastroenteritis in humans. The association of campylobacters with poultry is well established as a primary route for human exposure. The difference in normal core body temperature between chickens (42 degrees C) and humans (37 degrees C) has been suggested to trigger potential colonization or virulence factors and investigators have demonstrated differential gene expression at the two temperatures. Campylobacter spp. exhibit unique nutritional requirements and have been thought to only utilize amino acids and Kreb cycle intermediates as carbon sources for growth. We evaluated the ability of the genome-sequenced strain of Campylobacter jejuni 11168 (GS) to oxidize 190 different substrates as sole carbon sources at 37 degrees C and 42 degrees C using phenotype microarray (PM) technology. Results indicate that the expected amino acids, l-serine, l-aspartic acid, l-asparagine, and l-glutamic acid were utilized in addition to a number of organic acids. In general, oxidation of the substrates was greater at 42 degrees C than at 37 degrees C with a few exceptions. By employing the PM method, we observed a number of potential false-positive reactions for substrates including the triose, dihydroxyacetone; and the pentose sugars, d-xylose, d-ribose, l-lyxose, and d- and l-arabinose. The presence of genes possibly responsible for utilization of pentose sugars is supported by the genomic sequence data, but actual utilization as sole carbon sources for active respiration has not been observed. A better understanding of the metabolic pathways and nutritional requirements of campylobacters could lead to improvements in culture media for detection and isolation of the pathogen and to future intervention methods to reduce human exposure.
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PMID:Differential carbon source utilization by Campylobacter jejuni 11168 in response to growth temperature variation. 2003 8

Thermophilic Campylobacter species colonize the intestine of agricultural and domestic animals commensally but cause severe gastroenteritis in humans. In contrast to other enteropathogenic bacteria, Campylobacter has been considered to be non-glycolytic, a metabolic property originally used for their taxonomic classification. Contrary to this dogma, we demonstrate that several Campylobacter coli strains are able to utilize glucose as a growth substrate. Isotopologue profiling experiments with (13) C-labeled glucose suggested that these strains catabolize glucose via the pentose phosphate and Entner-Doudoroff (ED) pathways and use glucose efficiently for de novo synthesis of amino acids and cell surface carbohydrates. Whole genome sequencing of glycolytic C. coli isolates identified a genomic island located within a ribosomal RNA gene cluster that encodes for all ED pathway enzymes and a glucose permease. We could show in vitro that a non-glycolytic C. coli strain could acquire glycolytic activity through natural transformation with chromosomal DNA of C. coli and C. jejuni subsp. doylei strains possessing the ED pathway encoding plasticity region. These results reveal for the first time the ability of a Campylobacter species to catabolize glucose and provide new insights into how genetic macrodiversity through intra- and interspecies gene transfer expand the metabolic capacity of this food-borne pathogen.
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PMID:A transferable plasticity region in Campylobacter coli allows isolates of an otherwise non-glycolytic food-borne pathogen to catabolize glucose. 2625 68

The metabolic pathways of central carbon metabolism, glycolysis and oxidative phosphorylation (OXPHOS), are important host factors that determine the outcome of viral infections and can be manipulated by some viruses to favor infection. However, mechanisms of metabolic modulation and their effects on viral replication vary widely. Herein, we present the first metabolomics and energetic profiling of norovirus-infected cells, which revealed increases in glycolysis, OXPHOS, and the pentose phosphate pathway (PPP) during murine norovirus (MNV) infection. Inhibiting glycolysis with 2-deoxyglucose (2DG) in macrophages revealed that glycolysis is an important factor for optimal MNV infection, while inhibiting the PPP and OXPHOS showed a relatively minor impact of these pathways on MNV infection. 2DG affected an early stage in the viral life cycle after viral uptake and capsid uncoating, leading to decreased viral protein production and viral RNA. The requirement of glycolysis was specific for MNV (but not astrovirus) infection, independent of the type I interferon antiviral response, and unlikely to be due to a lack of host cell nucleotide synthesis. MNV infection increased activation of the protein kinase Akt, but not AMP-activated protein kinase (AMPK), two master regulators of cellular metabolism, implicating Akt signaling in upregulating host metabolism during norovirus infection. In conclusion, our findings suggest that the metabolic state of target cells is an intrinsic host factor that determines the extent of norovirus replication and implicates glycolysis as a virulence determinant. They further point to cellular metabolism as a novel therapeutic target for norovirus infections and improvements in current human norovirus culture systems.IMPORTANCE Viruses depend on the host cells they infect to provide the machinery and substrates for replication. Host cells are highly dynamic systems that can alter their intracellular environment and metabolic behavior, which may be helpful or inhibitory for an infecting virus. In this study, we show that macrophages, a target cell of murine norovirus (MNV), increase glycolysis upon viral infection, which is important for early steps in MNV infection. Human noroviruses (hNoV) are a major cause of gastroenteritis globally, causing enormous morbidity and economic burden. Currently, no effective antivirals or vaccines exist for hNoV, mainly due to the lack of high-efficiency in vitro culture models for their study. Thus, insights gained from the MNV model may reveal aspects of host cell metabolism that can be targeted for improving hNoV cell culture systems and for developing effective antiviral therapies.
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PMID:Glycolysis Is an Intrinsic Factor for Optimal Replication of a Norovirus. 3086 47