Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary tract infections activate a mucosal inflammatory response, which includes cytokine secretion and neutrophil influx. The mechanisms involved in the neutrophil influx have not been identified. Interleukin-8, a potent chemoattractant for neutrophils, is produced by urinary tract epithelial cell lines in vitro. This study analyzed the human IL-8 response to deliberate Escherichia coli infection of the urinary tract. Urine and serum samples were obtained before and after intravesical instillation of E. coli. Neutrophil numbers were determined on uncentrifuged urine, and IL-8 levels were measured by ELISA. A urinary IL-8 response was found in all patients after bacterial instillation, but no serum IL-8 was detected. There was a strong correlation between urinary IL-8 levels and urinary neutrophil numbers. The same E. coli strains used to colonize the patients stimulated IL-8 production in urinary tract epithelial cells. The level of IL-8 secreted by epithelial cell lines was influenced by the fimbrial properties of the E. coli. These results demonstrated that E. coli elicit a mucosal IL-8 response in humans, and suggested that IL-8 is involved in the onset of pyuria. Epithelial cells may be an important source of IL-8 during urinary tract infection.
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PMID:Interleukin-8 and the neutrophil response to mucosal gram-negative infection. 834 17

Urine and serum interleukin (IL)-6 and IL-8 responses were higher in children with febrile urinary tract infection (n = 61) than in those with asymptomatic bacteriuria (n = 39). By univariate analysis, cytokine levels were related to age, sex, reflux, renal scarring, urine leukocytes, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and bacterial properties (P fimbriae but not hemolysin). Multivariate modeling showed that urine IL-6 responses were higher in girls than boys, increased with age, and were positively associated with CRP, ESR, serum IL-6, and urine leukocyte counts. The urine IL-8 response was not influenced by age, but it was influenced by P fimbriae and was associated with ESR, CRP, urine leukocytes, and female sex. The results show that cytokine responses to urinary tract infection vary with the severity of infection and that cytokine activation is influenced by a variety of host and bacterial variables.
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PMID:Interleukin (IL)-6 and IL-8 in children with febrile urinary tract infection and asymptomatic bacteriuria. 889 12

We measured urinary endotoxin, IL-6 and IL-8 levels in 23 patients with gram-negative urosepsis. The endotoxin and cytokine levels showed a 100-1000 fold range. No correlation was found between levels of urinary endotoxin, and IL-6 or IL-8 levels. In all cases bacterial numbers were > or = 10(5) CFU ml-1 urine. The endotoxin content of the isolated microorganisms neither correlated with the urinary cytokine levels, nor with IL-6 and IL-8 levels obtained in vitro when 10(3) log-phase CFU of each of the bacteria were incubated with heparinized whole blood of three healthy donors. Neither the haemolysin phenotype of the bacteria, nor the presence of the P-pili gene was correlated with the cytokine response in vivo or in vitro. Other factors than known bacterial virulence factors apparently contribute to the wide variation in urinary cytokine levels in urinary tract infection.
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PMID:Known bacterial virulence factors do not explain the variation in urinary cytokine levels in patients with urosepsis. 911 47

Neutrophil accumulation in the graft kidney is a feature of cellular rejection and bacterial infection. The cellular infiltration is mediated by the local production of chemoattractant factors. The aim of the study was to analyze levels of IL-8 in renal graft recipients during and after episodes of acute renal rejection and urinary tract infection (UTI). A total of 50 renal graft recipients, including 10 with acute graft rejection (Group I) and 20 with UTI (Group II) were studied. Urine and serum levels of IL-8 were determined in patients of Group I before and after 7 days of antirejection therapy and in patients of Group II before and after 2 weeks of antimicrobial therapy. Results were compared with group of 20 patients with stable renal function and a group of 25 healthy people. IL-8 was determined by ELISA technique. The level of IL-8 in urine (uIL-8) was elevated in patients with acute graft rejection and uIL-8 decreased after antirejection treatment (772 +/- 241 pg/mg cr. vs 140 +/- 50 pg/mg cr.; p < 0.01). In 13 patients UTI was asymptomatic and 6 patients had an acute pyelonephritis. The level of uIL-8 was elevated in all patients with UTI and decreased after antimicrobial therapy. Levels of uIL-8 during acute pyelonephritis were significantly higher (p < 0.01) than in patients with asymptomatic bacteriuria (2582 +/- 950 pg/mg cr. vs 804 +/- 225 pg/mg cr.) Urine levels of IL-8 were lower in patients infected by Gram-positive Cocci as compared to patients infected by Gram-negative organisms. Patients with higher concentrations of serum creatinine during UTI had high urine levels of IL-8. Serum levels of IL-8 in patients of Group I and Group II were comparable with patients with stable graft function although they were higher than in control group. Elevated urinary secretion of IL-8 in acute rejection and UTI suggests a role of IL-8-neutrophiles system in in the pathogenesis in both inflammatory complications after kidney transplantation. Urine level of IL-8 was correlated with clinical symptoms of UTI.
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PMID:[Monitoring of interleukin-8 in urine and in serum of patients after kidney transplantation]. 1021 70

Interleukin (IL)-6 and -8 are important inflammatory cytokines in bacterial infections. Their serum and urine concentrations were measured in 27 neonates with urinary tract infection (UTI) at onset and the second week of therapy, as well as in 23 control neonates. Escherichia coli was isolated in 89% of cases. 99mTc-dimercaptosuccinic acid (99mTc-DMSA) scans were performed between the 10th and 90th days after UTI and showed pyelonephritic changes in 15 neonates (56%). Increased IL-6 and IL-8 concentrations were found in urine but not in serum within the first 24 h after presumptive diagnosis of UTI (P=.036 and.010, respectively), suggesting that the neonatal urinary tract can respond to uropathogens by producing inflammatory cytokines. Urine concentrations of IL-6 correlated with findings of renal changes in 99mTc-DMSA scans (P=.012) and thus may serve as a marker of renal parenchymal outcome. All neonates exhibited undetectable urine cytokine levels during the second week of therapy.
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PMID:Increased urine interleukin-6 concentrations correlate with pyelonephritic changes on 99mTc-dimercaptosuccinic acid scans in neonates with urinary tract infections. 1043 91

The urinary tract response to the entry of pathogens is complex and involves multiple aspects of the immune system. Herein we have divided them into cytokine, immunoglobulin, and cellular responses. Our current understanding suggests that interleukin 6 (IL-6) and IL-8 are the major contributors to the cytokine response. Both IL-6 and IL-8 are produced locally and systemically as part of the initiation of an inflammatory reaction. The cellular response becomes clinically apparent by the appearance of polymorphonuclear neutrophils (PMNs) in the urine. The contribution of gamma delta T-lymphocytes is beginning to be appreciated due to the use of gene-knockout mice in studies of urinary tract infection (UTI). B-lymphocytes are important because antibody response to UTI is important. In addition to the classic systemic antibody response, a local antibody response dominated by secretory immunoglobulin A (sIgA) has been shown to play a major role in the host response to UTI. Efforts to create a vaccine against UTI have focused on stimulation and intensification of this local sIgA production. Investigation continues to define the role of these responses, explain how they interact, and elucidate other aspects of the immune response to UTI that are yet unknown. Ultimately, this work aims to provide more effective treatment and prevention of UTI in those susceptible to invasions of the urinary tract by pathogens. Comprehension of how these responses interact may lead to a better understanding of UTI susceptibility and promote new and innovative types of treatment.
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PMID:The urinary tract response to entry of pathogens. 1065 65

Mucosal epithelial linings function as physical barriers against microbes. In addition, they participate in the first line of host defence by production of a variety of proinflammatory mediators when exposed to microbes and microbial agents. Here, we use a human urinary tract infection model to demonstrate that organ- and cell-specific innate responses induced by lipopolysaccharides (LPS) present on Gram-negative bacteria correlates with the expression of Toll-like receptor 4 (TLR4). The presence of TLR4 on human bladder epithelial cells enables them to rapidly respond to bacterial infections in vitro and in vivo. In contrast, TLR4 is not expressed on human proximal tubule cells isolated from the renal cortex, which may explain the cortical localization of bacteria in pyelonephritis. TLR4-negative renal epithelial cells, A498, are non-responsive to purified LPS, however, they respond to viable bacteria via a mannose-sensitive attachment-mediated pathway. To identify LPS components recognised by bladder epithelial cells, a bacterial lipid A mutant and LPS of different chemotypes were tested. Full interleukin 8 induction required hexa-acylated lipid A and was decreased by between 50% and 70% in the presence of O-antigen. Taken together, we propose that multiple independent pathways, which are organ- and cell-specifically expressed, mediate bacterial recognition and determine the outcome of innate responses to infection.
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PMID:Induction of innate immune responses by Escherichia coli and purified lipopolysaccharide correlate with organ- and cell-specific expression of Toll-like receptors within the human urinary tract. 1126 Jan 38

Uropathogenic Escherichia coli elicit a host response that determines the severity of urinary tract infection (UTI). Specific adherence mechanisms allow the bacteria to initiate this process by targeting epithelial cells in the urinary tract mucosa. Epidemiological studies show a strong association of P-fimbriae with disease severity, suggesting that adherence mediated by these organelles has a direct effect on mucosal inflammation in vivo. The present study examined the ability of P-fimbriae to induce inflammation in the human urinary tract. Patients were subjected to intravesical inoculation with a non-fimbriated E. coli strain or transformants of this strain expressing P-fimbriae. The inflammatory response was analysed as a function of P-fimbrial expression. The P-fimbriated transformants invariably caused higher interleukin (IL)-8, IL-6 and neutrophil responses in the urinary tract than the ABU strain. Furthermore, loss of P-fimbrial expression in vivo was accompanied by a return to background levels of neutrophils, IL-6 and IL-8 in individual patients. The results demonstrate that the pap sequences confer on a non-fimbriated, avirulent strain the ability to induce a host response in the human urinary tract. P-fimbriae thus fulfil the 'molecular Koch-Henle postulates' linking a single virulence factor to host response induction.
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PMID:P-fimbriae trigger mucosal responses to Escherichia coli in the human urinary tract. 1129 49

Urinary tract infections are common in infants and children. Pyelonephritis may result in serious complications, such as renal scarring, hypertension, and renal failure. Identification of the timing of release of inflammatory cytokines in relation to pyelonephritis and its treatment is essential for designing interventions that would minimize tissue damage. To this end, we measured urinary cytokine concentrations of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 in infants and children with pyelonephritis and in healthy children. Children that presented to our institution with presumed urinary tract infection were given the diagnosis of pyelonephritis if they had a positive urine culture, pyuria, and one or more of the following indicators of systemic involvement: fever, elevated peripheral white blood cell count, or elevated C-reactive protein. Urine samples were obtained at the time of presentation prior to the administration of antibiotics, immediately after completion of the first dose of antibiotics, and at follow up 12 to 24 h after presentation. IL-1 beta, IL-6, and IL-8 concentrations were measured by enzyme-linked immunosorbent assay. Creatinine concentrations were also determined, and cytokine/creatinine ratios were calculated to standardize samples. Differences between pre-antibiotic and follow-up cytokine/creatinine ratios were significant for IL-1 beta, IL-6, and IL-8 (P < 0.01). Differences between pre-antibiotic and control cytokine/creatinine ratios were also significant for IL-1 beta, IL-6, and IL-8 (P < 0.01). Our study revealed that the urinary tract cytokine response to infection is intense but dissipates shortly after the initiation of antibiotic treatment. This suggests that renal damage due to inflammation begins early in infection, underscoring the need for rapid diagnosis and intervention.
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PMID:Cytokine profiles of pediatric patients treated with antibiotics for pyelonephritis: potential therapeutic impact. 1168 40

The gram-negative bacterium Escherichia coli is the leading cause of urinary tract infection. The interaction between type 1 piliated E. coli and bladder epithelial cells leads to the rapid production of inflammatory mediators, such as interleukin-6 (IL-6) and IL-8. Conflicting reports have been published in the literature regarding the mechanism by which uroepithelial cells are activated by type 1 piliated E. coli. In particular, the role of lipopolysaccharide (LPS) in these responses has been an area of significant debate. Much of the data arguing against LPS-mediated activation of bladder epithelial cells have come from studies using a renal epithelial cell line as an in vitro model of the urinary epithelium. In this report, we analyzed three bladder epithelial cell lines and demonstrated that they all respond to LPS. Furthermore, the LPS responsivity of the cell lines directly correlated with their ability to generate IL-6 after E. coli stimulation. The LPS receptor complex utilized by the bladder epithelial cell lines included CD14 and Toll-like receptors, and signaling involved the activation of NF-kappaB and p38 mitogen-activated protein kinase. Also, reverse transcription-PCR analysis demonstrated that bladder epithelial cells express CD14 mRNA. Thus, the molecular machinery utilized by bladder epithelial cells for the recognition of E. coli is very similar to that described for traditional innate immune cells, such as macrophages. In contrast, the A498 renal epithelial cell line did not express CD14, was hyporesponsive to LPS stimulation, and demonstrated poor IL-6 responses to E. coli.
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PMID:CD14- and Toll-like receptor-dependent activation of bladder epithelial cells by lipopolysaccharide and type 1 piliated Escherichia coli. 1259 65


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