Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The regulation of intracellular concentrations of organic solutes, including glycine betaine, is an important adaptive response to osmotic stress for Escherichia coli. The clinical significance of glycine betaine to uropathogens is not clear. Clinical isolates of E. coli, Klebsiella pneumoniae, Enterobacter species, Pseudomonas aeruginosa, Proteus mirabilis, Staphylococcus aureus, S. saprophyticus, and Enterococcus faecalis accumulated glycine betaine from hyperosmotic media. The addition of glycine betaine to hyperosmotic minimal medium accelerated the growth rates of all species tested except P. mirabilis. However, when clinical strains of E. coli were transferred from urine with low osmolality to hyperosmotic urine, there was no slowing of the growth rate. There was no difference in growth rates of E. coli isolates from acute pyelonephritis, cystitis, and asymptomatic bacteriuria nor from fecal isolates. The ability to accumulate osmolytes, although it may be a factor in the adaptation to hypertonic environments, was not related to virulence.
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PMID:Is the ability of urinary tract pathogens to accumulate glycine betaine a factor in the virulence of pathogenic strains? 883 91

Osmoregulatory transporters ProP and ProU mediate the use of betaines as osmoprotectants by Escherichia coli. Glycine betaine and proline betaine are present in mammalian urines. Betaine uptake may therefore facilitate the growth of E. coli in the urinary tract, an environment of fluctuating osmolality. ProP transporter activity was approximately threefold higher in a pyelonephritis isolate, E. coli HU734, than in E. coli K-12. The growth rate of E. coli HU734 in aerated minimal salts medium was reduced twofold by 0.2 M NaCl in the absence and by 0.55 M NaCl in the presence of glycine betaine. Maximal growth rate stimulation was achieved when glycine betaine was added at a concentration as low as 25 microM. Deletion of the proP locus impaired the growth rate of E. coli HU734 in human urine but not in minimal medium supplemented with NaCl (0.4 M), with or without glycine betaine (0.1 mM). The expression of pyelonephritis-associated (P) pili was reduced when E. coli HU734 was cultured in a rich culture medium (LB) of elevated salinity. The proP lesion had no influence on P pilus expression in vitro or on the recovery of bacteria from the kidneys of inoculated mice. However, it did reduce their recovery from the bladders of inoculated mice 100-fold. These data provide the first direct evidence that osmoprotective betaine accumulation and transporter ProP are pertinent to both growth in human urine and colonization of the murine urinary tract by uropathogenic E. coli.
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PMID:Osmoregulatory transporter ProP influences colonization of the urinary tract by Escherichia coli. 946 1

Trehalose synthesis (RpoS-dependent) and betaine uptake mediated by transporters ProP and ProU contribute to the osmotolerance of Escherichia coli K-12. Pyelonephritis isolates CFT073 and HU734 were similar and diminished in osmotolerance, respectively, compared to E. coli K-12. The roles of RpoS, ProP and ProU in osmoregulation and urovirulence were assessed for these isolates. Strain HU734 expressed an RpoS variant which had low activity and a C-terminal extension. This bacterium accumulated very little trehalose and had poor stationary-phase thermotolerance. For E. coli CFT073, introduction of an rpoS deletion impaired trehalose accumulation, osmotolerance and stationary-phase thermotolerance. The rpoS defects accounted for the difference in osmotolerance between these strains in minimal medium of very high osmolality (1.4 mol kg(-1)) but not in medium of lower osmolality (0.4 mol kg(-1)). The slow growth of both pyelonephritis isolates in high-osmolality medium was stimulated by glycine betaine (GB) and deletion of proP and/or proU impaired GB uptake. An HU734 derivative lacking both proP and proU retained osmoprotective GB uptake activity that could be attributed to system BetU, which is not present in strain K-12 or CFT073. BetU transported GB (K(m), 22 microM) and proline betaine. High-osmolality human urine (0.92 mol kg(-1)) included membrane-permeant osmolyte urea (0.44 M) plus other constituents which contributed an osmolality of only approximately 0.4 mol kg(-1). Strains HU734 and CFT073 showed correspondingly low GB uptake activities after cultivation in this urine. Deletion of proP and proU slowed the growth of E. coli HU734 in this high-osmolality human urine (which contains betaines) but had little impact on its colonization of the murine urinary tract after transurethral inoculation. By contrast, deletion of rpoS, proP and proU had no effect on the very rapid growth of CFT073 in high-osmolality urine or on its experimental colonization of the murine urinary tract. RpoS-dependent gene expression is not essential for growth in human urine or colonization of the murine urinary tract. Additional osmoregulatory systems, some not present in E. coli K-12 (e.g. BetU), may facilitate growth of pyelonephritis isolates in human urine and colonization of mammalian urinary tracts. The contributions of systems ProP and ProU to urinary tract colonization cannot be definitively assessed until all such systems are identified.
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PMID:The osmotic stress response and virulence in pyelonephritis isolates of Escherichia coli: contributions of RpoS, ProP, ProU and other systems. 1139 Jun 97

Multiple transporters mediate osmoregulatory solute accumulation in Escherichia coli K-12. The larger genomes of naturally occurring strains such as pyelonephritis isolates CFT073 and HU734 may encode additional osmoregulatory systems. CFT073 is more osmotolerant than HU734 in the absence of organic osmoprotectants, yet both strains grew in high osmolality medium at low K(+) (micromolar concentrations) and retained locus trkH, which encodes an osmoregulatory K(+) transporter. Both lacked the trkH homologue trkG. Transporters ProP and ProU account for all glycine-betaine uptake activity in E. coli K-12 and CFT073, but not in HU734, yet elimination of ProP and ProU impairs the growth of HU734, but not CFT073, in high osmolality human urine. No known osmoprotectant stimulated the growth of CFT073 in high osmolality minimal medium, but putative transporters YhjE, YiaMNO, and YehWXYZ may mediate uptake of additional osmoprotectants. Gene betU was isolated from HU734 by functional complementation and shown to encode a betaine uptake system that belongs to the betaine-choline-carnitine transporter family. The incidence of trkG and betU within the ECOR collection, representatives of the E. coli pathotypes (PATH), and additional strains associated with urinary tract infection (UTI) were determined. Gene trkG was present in 66% of the ECOR collection but only in 16% of the PATH and UTI collections. Gene betU was more frequently detected in ECOR groups B2 and D (50% of isolates) than in groups A, B1, and E (20%), but it was similar in overall incidence in the ECOR collection and in the combined UTI and PATH collections (32 and 34%, respectively). Genes trkG and betU may have been acquired by lateral gene transfer, since trkG is part of the rac prophage and betU is flanked by putative insertion sequences. Thus, BetU and TrkG contribute, with other systems, to the osmoregulatory capacity of the species E. coli, but they are not characteristic of a particular phylogenetic group or pathotype.
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PMID:Osmoregulatory systems of Escherichia coli: identification of betaine-carnitine-choline transporter family member BetU and distributions of betU and trkG among pathogenic and nonpathogenic isolates. 1470 97

Urinary tract infections (UTIs) are among the most common infections caused by microorganisms, and pyelonephritis is the most severe infection of the urogenital tract. The risk of developing chronic renal insufficiency due to a UTI without other risk factors is low. The pathogenicity and virulence of the infective microorganisms as well as the efficiency of local or systemic defence mechanisms determine the course and severity of the disease. Virulence properties (adhesins, toxins, capsule, iron uptake) are encoded by genomic structures and the determination of virulence is influenced by the host situation. In renal insufficiency, a variety of quite different substances (uraemic toxins, betaine, amino acids, creatinine, urea, glucose) influence the microbial environment. Defence factors (Tamm-Horsfall protein, defensin, phagocytic activity of granulocytes) and underlying anatomical lesions as well as pre-existing renal disease determine the severity of UTI and the prognosis of renal insufficiency.
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PMID:The interaction of urinary tract infection and renal insufficiency. 1684 55