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

Cytokines may play an important role in the regulation of host defense against local bacterial infections. We have evaluated the local production of cytokines in a BALB/c mouse model of Escherichia coli pyelonephritis. Kidneys, draining lymph nodes, and spleens, were harvested at specific time intervals after bladder inoculation with E. coli corresponding to the stages of renal infection, infiltration, and bacterial clearance seen in this model. The presence of messenger RNA for specific cytokines (interleukins 1 through 6, chemotactic factors, granulocyte and granulocyte macrophage-colony stimulating factor (GM-CSF), tumor necrosis factor (TNF alpha) and beta, IFN gamma, transforming growth factor (TGF beta), and cytokine synthesis inhibitory factor (CSIF)/IL-10) was determined by polymerase chain reaction (PCR) amplification of reverse transcribed RNA. We have demonstrated mRNA encoding IL-1, IL-6, G-CSF, GM-CSF, TNF alpha, H400 (a protein homologous to a family of chemotactic factors and identical to MIP-1 beta), and CSIF/IL-10 in the kidney at 12 h and 1, 2, and 3 d after bacterial challenge. No signal was seen in normal animals or in mice after 5 d. This pattern of cytokine expression was observed only in renal tissues suggesting a localized response. IL-6 was present in the urine at 4 h with rapid resolution to baseline levels by 24 to 48 h. In contrast, IL-6 was not usually detectable in the serum. TNF alpha was not detectable in the serum or urine during the course of the infection. By immunohistochemical staining of kidney sections we have shown that IL-6 is produced predominantly by mesangial cells rather than by the inflammatory infiltrate. This study provides additional evidence utilizing novel techniques that specific cytokines are produced locally in response to bacterial infections. The time course of production demonstrated in this model supports the important role of cytokines in natural host resistance to local infection.
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PMID:Local cytokine production in a murine model of Escherichia coli pyelonephritis. 154 64

Urine and serum concentrations of interleukin (IL)-6 and IL-8 were determined in 43 women with acute pyelonephritis caused by Escherichia coli. Urine and serum samples were also collected 2 weeks after the infection and during a subsequent episode of cystitis (n = 8) or asymptomatic bacteriuria (n = 8). Concentrations of IL-6 and IL-8 were related to the expression of 5 virulence markers of E. coli and glomerular filtration rate (GFR) after pyelonephritis. Patients with acute pyelonephritis had elevated urine and serum IL-6 and IL-8 levels as compared to 37 healthy women (IL-6: p < 0.001 in both cases, and IL-8: p < 0.001 in both cases). Patients infected with E. coli producing hemolysin and/or cytotoxic necrotizing factor (CNF) had significantly higher IL-6 levels in serum during acute pyelonephritis as compared to patients infected with strains without the ability to produce these factors (p = 0.0025 and p = 0.0154, respectively). Patients who had high concentrations of IL-8 in urine during acute pyelonephritis had lower GFR at follow-up as compared to patients with lower levels of IL-8 in urine (r = -0.48, p = 0.0123). In conclusion, acute pyelonephritis is accompanied by elevated urinary and serum IL-6 and IL-8 levels. Bacteria producing hemolysin and CNF seem to induce higher concentrations of IL-6 in serum. The secretion of IL-8 from renal cells may participate in the initiation and maintenance of renal inflammation which in turn may influence renal function.
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PMID:Interleukin-6 and interleukin-8 in serum and urine in patients with acute pyelonephritis in relation to bacterial-virulence-associated traits and renal function. 791 3

Experimental acute pyelonephritis in monkeys led to death in some of the animals following renal E. coli inoculation. It was found that both the inflammatory response and cytokine activation were much more severe in these monkeys as compared with others that survived. IL-1 was decreased just before death, and there were early increases in IL-2 and IL-6 serum concentrations, but no significant increase in TNF values. The data suggest that death in sepsis is due in part to excessive cytokine release because of a decrease in the protective activity of IL-1.
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PMID:Events leading to septic death from experimental acute pyelonephritis in the monkey. 834 80

In the pathogenesis of glomerulonephritis, acute renal failure, pyelonephritis and other diseases of the kidneys oxygen radicals are involved. Some types of glomerulonephritis are characterized by infiltration of the glomeruli by neutrophils and monocytes which can form oxygen radicals (superoxide, hydrogen peroxide). The increased amount of cAMP in glomeruli can be due to oxygen radicals. Cyclic nucleotides modulate the inflammatory or immune response in glomerular disease and play a part in the action of local mediators of the inflammation. Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Radicals formed by the system myeloperoxidase--hydrogen peroxide--halogen derivatives activate proteolytic enzymes (proteinases) which break down collagen and other components of the extracellular matrix present in the basal membrane of glomeruli and in the mesangium. Oxygen radicals and proteinases can cause and amplify glomerular damage. Glucocorticoid administration leads to an increased activity of endogenous antioxidant enzymes in the glomerulus and reduced the of lipid peroxidation.
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PMID:[The role of oxygen radicals in the pathogenesis of glomerulonephritis]. 859 8

We compared the urinary concentrations of soluble TNF-I (sTNF-RI), TNF-II receptors, and soluble IL-6 receptor (sIL-6R) standardized to urinary creatinine concentrations, in children with acute pyelonephritis, in children with non-renal fever and in healthy controls. These levels were related to the acute inflammatory response in the kidneys and later renal scarring, as determined by acute and 1-y follow-up with 99mTC-dimercaptosuccinic acid scintigraphy (DMSA). The concentrations of the soluble receptors were measured using enzyme immunoassay (EIA). The urinary levels of sTNF-RI were significantly higher in children with acute pyelonephritis (median 1320 pg/mmol) than in children with non-renal fever, children 6 weeks after acute pyelonephritis and healthy controls (873, 251 and 477 pg/mumol, respectively). Median sTNF-RII urine levels were also higher in acute pyelonephritis (4123 pg/mumol) than in the three control groups (2000, 964 and 1850 pg/mumol, respectively). In contrast, the highest urinary sIL-6R concentrations were found in healthy children (median 420 pg/mumol), compared to those with acute pyelonephritis (235 pg/mumol), children with non-renal fever and children 6 weeks after pyelonephritis (137 and 50 pg/mumol, respectively). No significant difference was found in any of the urinary soluble receptor levels in children with or without DMSA uptake defects at the acute or the 1-y follow-up scintigraphy. In conclusion, although the urinary soluble TNF receptor levels were higher during acute pyelonephritis, this observation was not useful for deciding which children needed follow-up after acute pyelonephritis.
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PMID:Soluble receptors to tumour necrosis factor and interleukin-6 in urine during acute pyelonephritis. 940 13

The aim of this study was to investigate the influence of IL-6 on mortality, bacterial growth and cytokine expression in experimental acute pyelonephritis. Female IL-6-deficient mice and their wild-type counterparts, 8-10 weeks old, were infected with Escherichia coli CFT 073 or injected with NaCl 0.9% (w/v) via the urethra and thereafter obstructed for 6 h. Animals were killed at 48 h, 6 days or 8 weeks and cytokine and bacterial renal levels were assessed at each time point. We found that IL-6-deficient mice had increased mortality and extensive renal bacterial growth on day 6, compared with wild-type mice (P < 0.05) and the histopathological changes were generally more severe and widespread in the IL-6-deficient mice. Peak mRNA expression of IL-1beta, IL-4, IL-10, IL-12 and interferon-gamma (IFN-gamma) occurred 48 h after infection in both IL-6 knock out and wild-type mice. Transforming growth factor-beta (TGF-beta) levels also peaked at 48 h in E. coli-infected wild-type mice, while in the IL-6-deficient strain both TGF-beta mRNA and protein levels were significantly lower at 48 h than wild-type levels (P < 0.0008 and P < 0.03, respectively) and remained stationary throughout the study period. Animals injected with NaCl 0.9% (w/v) displayed a similar decrease in TGF-beta expression (P < 0.02). When splenocytes from the IL-6-deficient mice were incubated with murine recombinant IL-6, TGF-beta levels increased to those of wild-type mice. No increase was observed when splenocytes from wild-type mice were incubated with the same doses of rIL-6. We therefore conclude that IL-6 plays an important role in bacterial clearance and directly influences the TGF-beta levels in experimental acute pyelonephritis. We also demonstrate that urethral obstruction per se induces an increase in TGF-beta the magnitude of which is decreased in IL-6-deficient mice.
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PMID:Renal cytokine responses in acute Escherichia coli pyelonephritis in IL-6-deficient mice. 1109 Dec 75

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

Renal scarring after pyelonephritis is common in infancy. In this experimental study performed on tissue from 10-d-old infant and 40-d-old pubertal rats, several aspects of the renal innate immune response to a pyelonephritogenic strain of alpha-hemolysin-expressing Escherichia coli were compared. The kidney typically responds to urinary tract infection with release of proinflammatory cytokines, e.g. IL-6. Basal production of IL-6 from 10-d-old renal cortical tissue was approximately 20% of that from 40-d-old tissue. Six-hour incubation in the presence of supernatant from the E. coli culture caused an approximately 15-fold increase of IL-6 release in 10-d-old tissue and a 5-fold increase in 40-d-old tissue. The absolute level of IL-6 release in stimulated tissue was, however, significantly lower at 10 d than at 40 d. Lipopolysaccharide, the most immunogenic component of E. coli, signals via Toll-like receptor 4. Reverse transcriptase PCR performed on outer renal cortex indicated that expression of Toll-like receptor 4 mRNA was similar in both ages. Microdissection studies revealed that Toll-like receptor 4 mRNA was expressed in proximal tubules but not in glomeruli. The exotoxin alpha-hemolysin, expressed by a majority of uropathogenic E. coli isolates, stimulates IL-6 release via an alternative pathway that signals via intracellular calcium oscillations. We conclude that the higher susceptibility to pyelonephritic scarring is unlikely related to immaturity of innate immune system, as measured by cellular release of IL-6. Instead, the underlying mechanisms for pyelonephritic scarring are most likely multifactorial and may be mainly attributed to anatomic immaturity of the urinary tract.
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PMID:Developmental aspects of Escherichia coli-induced innate responses in rat renal epithelial cells. 1284 Jan 57

This prospective study, performed in 76 children with a urinary tract infection (UTI), evaluates the diagnostic value of procalcitonin (PCT) and proinflammatory cytokines (IL-1beta, IL-6 and TNF-alpha) in children with acute pyelonephritis documented by dimercaptosuccinic acid scintigraphy (DMSA). Renal parenchymal involvement was assessed by (99m )Tc-DMSA scintigraphy within 7 days of admission. The diagnosis of acute pyelonephritis was confirmed only in patients with reversible lesions on scintigraphy. According to DMSA scan results, patients were divided into two groups, lower UTI or acute pyelonephritis. In acute pyelonephritis, serum PCT level was found to be significantly higher than it is in the lower UTI (p <0.001). Also, significantly higher serum proinflammatory cytokines (IL-1beta, IL-6 and TNF-alpha) levels were detected in those with acute pyelonephritis than those with lower UTI (p <0.001). We conclude that both serum PCT and proinflammatory cytokine levels may be used as accurate markers for diagnosis of acute pyelonephritis.
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PMID:Proinflammatory cytokines and procalcitonin in children with acute pyelonephritis. 1607 86

The aim of this prospective study was to examine gender-related differences of cytokines in the plasma and urine of healthy individuals that might provide a clue concerning the lower rate of chronic renal diseases in females. Soluble interleukin-1 receptor antagonist (sIL-1RA), interleukin (IL)-1alpha, IL-1beta, IL-2, sIL-2R, IL-3, IL-4, IL-6, sIL-6R, IL-10, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta(2) and interferon (IFN)-gamma were determined using standard enzyme-linked immunosorbent assay (ELISA). Cytokine levels were determined in simultaneously obtained plasma and urine samples of 18 male and 28 female healthy members of our laboratory staff. Urine cytokine levels were studied three times at 1-month intervals. All individuals had a negative urine nitrite test and showed no symptoms of urinary tract infection (UTI). Plasma levels of all studied cytokines were similar in males and females (P = n.s.). However, females had significantly higher urine IL-1alpha (P < 0.0001; P < 0.0001; P < 0.0001) and sIL-1RA (P = 0.0001; P = 0.0003; P = 0.0002) than males at three and higher IL-1beta at one of the three investigations (P = 0.098; P = 0.003; P = 0.073). Urine levels of the other cytokines were similar in males and females. Higher urine levels of IL-1alpha, IL-1beta and sIL-1RA in females may result from stimulation of cells in the urinary tract. Increased sIL-1RA might block T lymphocyte activation. The elevated cytokines may play a role in the protection of the female urinary tract from certain renal diseases, such as pyelonephritis and other inflammatory and sclerotic kidney diseases.
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PMID:Strikingly higher interleukin (IL)-1alpha, IL-1beta and soluble interleukin-1 receptor antagonist (sIL-1RA) but similar IL-2, sIL-2R, IL-3, IL-4, IL-6, sIL-6R, IL-10, tumour necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta and interferon IFN-gamma urine levels in healthy females compared to healthy males: protection against urinary tract injury? 1623 18


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