Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The host-response parameters fever, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) are activated in concert by cytokines such as interleukin-6 (IL-6). Il-6 is secreted in response to Escherichia coli infection of the urinary tract. This study tested the hypothesis that the level of fever, CRP, and ESR is coregulated in individual patients. Body temperature, CRP, ESR, pyuria, and renal concentrating capacity were analyzed in 692 children with first-time urinary tract infections. The association of the parameters was evaluated by correlation and multiple regression analysis. The body temperature, CRP, and ESR were significantly correlated (r = .54, .58, and .58; P less than .001), and variation in CRP and ESR explained approximately 40% of the variation in fever. In contrast, the renal concentrating capacity and pyruia were weakly or not at all correlated with the febrile response (r = -.22; P less than .001), and less than 10% of the variation in renal concentrating capacity was explained by the other parameters. The results suggest that fever, CRP, and ESR describe the same aspect of the host response to UTI.
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PMID:Dependence among host response parameters used to diagnose urinary tract infection. 198 17

Escherichia coli (E. coli) causes greater than 90% of urinary tract infections, UTI, in childhood. The capacity to adhere to urinary tract epithelial cells characterizes E. coli strains that cause acute pyelonephritis. Adherence of uropathogenic E. coli is the result of a specific interaction between bacterial adhesins and glycolipid receptors on the host cells, especially the globoseries of glycolipids which share the Galactose alpha 1-greater than 4Galactose beta disaccharide (Gal alpha 1-greater than 4Gal beta). In childhood UTI, Gal alpha 1-greater than 4Gal beta-binding bacteria caused significantly higher body temperature, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and pyuria, and lower renal concentrating capacity, than E. coli lacking this specificity. The Gal alpha 1-greater than 4Gal beta-binding bacteria thus appeared to be more potent inducers of inflammation than other strains. Since inflammation may lead to tissue damage we examined the relationship of infection with Gal alpha 1-greater than 4Gal beta-positive bacteria to renal scarring. The frequency of renal scarring was 5% in boys with Gal alpha 1-greater than 4Gal beta-positive and 40% in boys with Gal alpha 1-greater than 4Gal beta-negative E. coli. Bacterial binding to Gal alpha 1-greater than 4Gal beta can be detected with a commercially available test reagent. This reagent can thus be used as an effective predictor of risk for renal scarring. Interleukin-6 (IL-6) is a pyrogen and inducer of the acute phase reactants. It was shown to be produced locally in the urinary tract, in response to UTI, and to spread systemically. Mucosal challenge with dead bacteria was sufficient to induce the IL-6 response. Circulating IL-6, and/or IL-1 and tumor necrosis factor could explain the fever, as well as increased ESR and CRP found in association with acute symptomatic UTI.
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PMID:Bacterial adherence as a virulence factor in urinary tract infection. 228 1

Kawasaki disease (KD) often presents with abnormal urinary findings, such as aseptic pyuria, mild proteinuria and microscopic haematuria. In this study, we measured urinary interleukin-6 (IL-6) by a sensitive sandwich ELISA assay using mouse monoclonal antibodies against recombinant IL-6 to elucidate the role of IL-6 in the pathogenesis of renal lesions in KD. Serum IL-6 levels were increased in acute KD as well as in febrile controls. Importantly, urinary IL-6 levels were consistently elevated in patients with acute KD, but much lower in febrile controls. Urinary IL-6 levels returned steadily to normal during the convalescent phase. In addition to IL-6, urinary levels of N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (beta 2-mg) were also elevated during the acute phase of this disease. Eosinophils and macrophages were identifiable in urinary sediments from these patients. The increased levels of urinary IL-6 in combination with increased NAG and beta 2-mg seemed to suggest the presence of certain renal parenchymal lesions with cellular infiltration during the acute phase of the disease. IL-6 may serve as clinically useful parameter for the detection and monitoring of the renal involvement in KD.
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PMID:Increased levels of urinary interleukin-6 in Kawasaki disease. 840 68