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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The response of circulating and infected kidney lymphocytes to the O (lipopolysaccharide) and K (polysaccharide) antigens of an Escherichia coli O6 K 13 H1 strain was determined. Both circulating and kidney lymphocytes showed significant incorporation of [3H-methyl]thymidine into DNA when incubated with the O antigen, whereas neither responded to the K antigen. The lipid moiety of the lipopolysaccharide was required for lymphocyte responsiveness. Upon sequential incubation of O antigen and fluoresceinated homologous antiserum, 24-30 per cent of kidney lymphocytes were shown to have surface receptors for O antigen, whereas none had surface receptors for K antigen. Although the K antigen is an important determinant of invasiveness of the upper urinary tract, it fails to elicit a cellular immune response or attach to lymphocytes from the infected kidney in experimental pyelonephritis.
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PMID:Local immunie response in experimental pyelonephritis in the rabbit. III. Lymphocyte responsivieness to O and K antigens of Escherichia coli. 78 43

The cellular activity of circulating lymphocytes and lymphocytes isolated from the infected kidney of animals with experimental haematogenous pyelonephritis was evaluated. The incorporation of [3H-methyl]thymidine into DNA by lymphocytes was studied with mitogens such as phytohaemagglutinin (PHA), pokeweek mitogen (PWM) and goat anti-rabbit IgG (GARIG). Lymphocytes from infected kidney had a high baseline DNA synthesis compared to circulating lymphocytes from days 5 to 27 of infection. Infected kidney lymphocytes failed to respond to PHA, PWM, or GARIG, whereas circulating lymphocytes did respond to these mitogens. Uropod-bearing lymphocytes, which were shown to be T lymphocytes, were present from days 5 to 77 of infection. B lymphocytes, as determined by surface immunofluorescent technique, were present by day 12, coincident with the onset of local synthesis of antibody. These studies reveal that in pyelonephritis, the cellular response goes through sequential changes and indicate a dynamic interrelationship between T and B lymphocytes at an infected site.
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PMID:Local immune response in experimental pyelonephritis in the rabbit. I. Morphological and functional features of the lymphocytic infiltrate. 108 92

A population of fast sedimenting spleen cells was identified as the cause of impaired in vitro response of spleen cells to concanavalin A (Con A) in acute pyelonephritis in rats. These fast-sedimenting cells responded to Con A by suppressing the DNA synthetic response of normal spleen cells to Con A. In addition, spleen cells from acute pyelonephritis rats were significantly less able to mediate in vitro cell destruction in xenogeneic aggressor lymphocyte: target L cell mixtures. On the basis of these findings, the hypothesis is proposed that a suppressor cell can protect the pyelonephritic kidney against immunologically mediated tissue damage.
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PMID:Cellular immunity in pyelonephritis: identification of suppressor cell activity of spleen cells in response to concanavalin A and inhibition of lymphocyte-mediated L cell cytotoxicity. 108 93

Adhesin-encoding operons (pap, sfa/foc, and afa) have been shown to be prevalent in Escherichia coli strains associated with urinary tract infections. A quick and sensitive assay to identify these operons was developed by using the polymerase chain reaction (PCR). Three pairs of 25-mer primers were defined from the sequences of the DNA fragments used as probes in hybridization studies to identify each of the three operons, and the six primers were used together in a single reaction of amplification. To validate the PCR approach for detection of adhesin-encoding operons among clinical isolates, we investigated a collection of 97 E. coli isolates with the following characteristics: all isolates originated from the urine of patients with pyelonephritis, and the adhesin responsible for specific binding of the isolates to uroepithelial cells was previously characterized by phenotypic assays, as well as genotypic tests based on hybridization. There was a perfect correlation between the results obtained with the PCR approach and those previously obtained by using DNA probes. These results indicate that the PCR method, which is highly specific and easier to perform than the hybridization method, is a powerful genotypic assay for detection of adhesin-encoding operons. Thus, this assay can be recommended for clinical use to detect virulent urinary E. coli strains, as well as for epidemiological studies.
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PMID:Rapid and specific detection of the pap, afa, and sfa adhesin-encoding operons in uropathogenic Escherichia coli strains by polymerase chain reaction. 134

Pyelonephritis-associated pilus (Pap) expression is regulated by a phase variation control mechanism involving PapB, Papl, catabolite activator protein (CAP), leucine-responsive regulatory protein (Lrp) and deoxyadenosine methylase (Dam). Lrp and Papl bind to a specific non-methylated pap regulatory DNA region containing the sequence 'GATC' and facilitate the formation of an active transcriptional complex. Evidence indicates that binding of Lrp and Papl to this region inhibits methylation of the GATC site by Dam. However, if this GATC site is first methylated by Dam, binding of Lrp and Papl is inhibited. These events lead to the formation of two different pap methylation states characteristic of active (ON) and inactive (OFF) pap transcription states. The fae (K88), daa (F1845) and sfa (S) pilus operons share conserved 'GATC-box' domains with pap and may be subject to a similar regulatory control mechanism involving Lrp and DNA methylation.
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PMID:Evidence for global regulatory control of pilus expression in Escherichia coli by Lrp and DNA methylation: model building based on analysis of pap. 135 27

E. coli strain 536 (O6:K15:H31) isolated from a case of acute pyelonephritis, expresses S-fimbrial adhesins, P-related fimbriae, common type I fimbriae, and hemolysins. The respective chromosomally encoded determinants were cloned by constructing a genomic library of this strain. Furthermore, the strain produces the iron uptake substance, enterocheline, damages HeLa cells, and behaves in a serum-resistant mode. Genetic analysis of spontaneously arising non-hemolytic variants revealed that some of the virulence genes were physically linked to large unstable DNA regions, termed "pathogenicity islands", which were mapped in the respective positions on the E. coli K-12 linkage map. By comparing the wild type strain and mutants in in vitro and in vivo assays, virulence features have been evaluated. In addition, a regulatory cross talk between adhesin determinants was found for the wild-type isolate. This particular mode of virulence regulation is missing in the mutant strain.
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PMID:Genetics of Escherichia coli uropathogenicity: analysis of the O6:K15:H31 isolate 536. 155 5

Multiple isolates of Escherichia coli from the blood and urine of a 60-year-old woman with acute pyelonephritis exhibited different biotypes, antimicrobial susceptibility patterns, and plasmid profiles, suggesting the presence of polymicrobial bacteriuria and leaving in question the origin of the bacteremia. Only after bacterial restriction endonuclease analysis of total bacterial DNA was it discovered that all isolates represented the same strain, with plasmid instability possibly accounting for the varied antimicrobial susceptibility patterns observed. We conclude that the biotype, antimicrobial susceptibility profile, and plasmid profile are sometimes inadequate to clarify the relationships between different clinical isolates of E. coli from a single patient and can lead to erroneous epidemiologic conclusions. DNA fingerprinting can resolve dilemmas these less precise techniques leave unresolved.
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PMID:Success of DNA fingerprinting after failure of biotyping, antimicrobial susceptibility testing, and plasmid analysis to reveal clonality of multiple blood and urine isolates from a patient with Escherichia coli urosepsis. 164 17

Oxidant injury has been implicated in the pathogenesis of inflammatory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likely to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.
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PMID:Reactive oxygen molecules, oxidant injury and renal disease. 166 82

Transcription of the pyelonephritis-associated pilus (pap) operon of Escherichia coli is subject to regulation by a phase variation control mechanism in which the pap pilin gene alternates between transcriptionally active (phase-on) and inactive (phase-off) states. Pap phase variation appears to involve differential inhibition of deoxyadenosine methylase (Dam) methylation of two pap GATC sites, GATC1028 and GATC1130, located in the regulatory region upstream of the papBA promoter. DNA from phase-on cells contains an unmethylated adenosine in the GATC1028 site, whereas DNA from phase-off cells contains an unmethylated adenosine in the GATC1130 site. papI and papB are two regulatory genes in the pap operon. Analysis of pap deletion mutants suggests that papI is required for methylation inhibition at the GATC1028 site; however, neither papI nor papB is required for inhibition of methylation at the GATC1130 site. We have identified a chromosomal locus, mbf (methylation-blocking factor), that is required for methylation protection of both the pap GATC1028 and GATC1130 sites. The mbf locus was identified after transposon mTn10 mutagenesis and mapped to 19.6 min on the E. coli chromosome. The effect of transposon mutations within mbf on pap pilin transcription was determined by using a papBAp-lac operon fusion which places lacZ under control of the papBA promoter. E. coli containing mbf::mTn10 and phase-off mbf+ E. coli cells both expressed beta-galactosidase levels about 30-fold lower than the beta-galactosidase level measured for phase-on mbf+ E. coli cells. These results indicated that mbf was necessary for pap pilin transcription and were supported by Northern (RNA) blotting and primer extension analyses. Moreover, transposon insertion within mbf greatly reduced Pap pilus expression. The mbf locus was isolated on a low-copy-number cosmid, pMBF1. Complementation analysis indicated that each of seven mbf::mTn10 mutants isolated contained a transposon insertion within the same gene or operon. The identification of the mbf locus, required for pap transcription, supports the hypothesis that pap phase variation is controlled by a mechanism involving alternation between different methylation states.
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PMID:Evidence for a methylation-blocking factor (mbf) locus involved in pap pilus expression and phase variation in Escherichia coli. 167 57

The frequency of Escherichia coli with Gal alpha 1-4Gal beta-specific adhesins is reduced among children who develop renal scars. The adhesion-negative phenotype may be due to the absence of the pap DNA sequences which encode these adhesins or to a phase variation event induced by in vitro culture. In the present study the frequency of pap and pil homologous DNA was determined by dot blot analysis with probes specific for the respective sequence using E. coli strains from children with recurrent pyelonephritis with and without renal scarring. The frequency of pap was 79% in the strains isolated from the nonscarring group compared with 39% in the strains from the scarring group (P less than 0.001). The Gal alpha 1-4Gal beta phenotype was expressed by 89% of the pap-positive strains from the nonscarring group compared with 71% in the scarring group (P less than 0.05). In addition 13 of 77 of the pap-positive E. coli strains agglutinated sheep erythrocytes but not the Gal alpha 1-4Gal beta latex beads; a reaction attributed to reactivity with the Forssman glycolipid. DNA sequences homologous with pil were found in 95% of all strains and there was no significant difference between the nonscarring and the scarring groups. The low frequency of Gal alpha 1-4Gal beta specific strains in the scarring group was therefore due to the absence of pap-homologous DNA sequences and to a reduced rate of phenotypic expression among pap-positive scarring strains. There was no support for a relationship between type 1 fimbriae and renal scarring.
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PMID:Escherichia coli in patients with renal scarring: genotype and phenotype of Gal alpha 1-4Gal beta-, Forssman- and mannose-specific adhesins. 167 31


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