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)

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

We reported the prophylactic and therapeutic effect of human granulocyte-colony stimulating factor (G-CSF) on mice with ascending pyelonephritis induced by Pseudomonas aeruginosa (G-group). In the cyclophosphamide-treated neutropenic mice, the prophylactic administration of G-CSF (2 micrograms/day/mouse) yielded a lower incidence of infection than that of saline alone. However, the therapeutic administration of G-CSF (2 micrograms/day/mouse) did not produce decreases of the rate, suggesting that this type of administration had no effect on infection. Thus, we investigated the effect of the combination therapy of G-CSF and Amikacin. In neutropenic mice, the therapeutic administration of G-CSF alone and Amikacin (20 mg/kg) alone did not produce decreases of incidence of infection. But, combination administration of these yielded a lower incidence of infection. These results suggest that synergy of bactericidal effects of neutrophils accelerated by G-CSF with Amikacin, and a combination of these have a therapeutic effect on bacterial infection in neutropenic mice.
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PMID:[Study of the effect of combination therapy of human granulocyte-colony stimulating factor (G-CSF) and amikacin on experimental pyelonephritis induced by Pseudomonas aeruginosa in neutropenic mice]. 169 97

We investigated the prophylactic and therapeutic effect of human granulocyte-colony stimulating factor (G-CSF) on mice with ascending pyelonephritis induced by Pseudomonas aeruginosa (G-group). This experimental model was established by a two course administration of cyclophosphamide, so that it kept the mice in a neutropenic status (around 2000 white blood cells/mm3) from the time of infection to the time of sacrifice. The cyclophosphamide-treated group increased their susceptibility more than the control group. In the cyclophosphamide-treated group, the prophylactic administration of G-CSF (2 micrograms/day/mouse) yielded a lower incidence of infection and of infection-induced mortality than that of saline alone. However, the therapeutic administration of G-CSF did not produce significant decreases of these rates, suggesting that this type of administration had no effect on infection. At the time of sacrifice, the prophylactic administration of G-CSF increased the number of neutrophils, while at the time of induced infection, no increase of neutrophils was found. G-CSF therapeutic administration was not able to increase neutrophils during the experiment. An investigation of the bacterial capacity of peritoneal exudate neutrophils revealed that G-CSF prophylactic administration accelerated its capacity, although cyclophosphamide alone did not. These results suggest that G-CSF has a prophylactic effect on bacterial infection in neutropenic mice, and that this effect, in part, depends upon both the increase of neutrophils and the acceleration of bactericidal capacity produced by G-CSF.
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PMID:[Study of the prophylactic and therapeutic effect of human granulocyte-colony stimulating factor (G-CSF) on experimental pyelonephritis induced by pseudomonas aeruginosa in neutropenic mice]. 247 50

Diabetic patients are said to be prone to infections. Several studies of different host defense mechanisms report defects in individual granulocyte functions and cell mediated immunity, especially in patients with poorly controlled diabetes. Diabetic females have an increased risk of developing urinary tract infections. This high susceptibility is probably due to local risk factors such as diabetic cystopathy and vaginitis, the latter being frequently associated with glucosuria. Urinary tract infections in diabetic individuals often have a complicated course which may be explained by the aforementioned compromised host defense mechanisms. Diabetics have an increased risk not only of lower, but also of upper urinary tract infections. Urinary tract infections such as emphysematous cystitis and pyelonephritis, as well as papillary necrosis as a complication of pyelonephritis, are not uncommon in diabetic patients. Rapid recognition and management of such complicated urinary tract infections is important.
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PMID:[Urinary tract infection in the diabetic patient]. 637 86

Renal scars have been thought to occur only in later stages of chronic pyelonephritis. In our experimental pyelonephritis model, bacteria with mannose-sensitive (MS) pili on its surface promoted renal scarring when inoculated into renal parenchyma. Pretreatment with recombinant human granulocyte-colony-stimulating factor (rhGCSF) inhibited the renal scarring which followed inoculation with MS-piliated bacteria, whereas posttreatment at an early stage of infection had no effect on renal scarring. These findings suggest that rhGCSF may be useful for the prevention of infection without increasing the tissue damage to the renal parenchyma which leads to the renal scarring. Even when rhGCSF is used for treatment of kidney infection, it does not promote increased renal scarring through the increased invasion of leukocytes at the inflammatory site.
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PMID:Effect of recombinant human granulocyte-colony-stimulating factor on renal scarring following infection with MS-piliated bacteria. 768 31

The close similarities between the urinary tract of primates make it possible to use the monkey as a model for understanding the pathophysiology of pyelonephritis in the human. Basically, experimental protocols consist in introducing uropathogenic strains of E. coli into the bladder and/or the ureter in the monkey and to determine early and late consequences of the subsequent renal tissue infection. Lesions appear within the first minutes of bacterial invasion. They result from the virulence of the parasite, which pertains to multiple factors, with a prominent role of fimbrial adhesion. However, the defense mechanisms of the host better explain the renal tissue insult. They comprise early ischoemia due to granulocyte aggregation within the renal capillaries, followed by damage due to oxygen free radicals which are generated during reperfusion. The primate model of pyelonephritis is extremely useful to understand most clinical, functional and radiological events observed in the course of human pyelonephritis. This model also serves to test pharmacological manoeuvres aimed at preventing the renal tissue injury of pyelonephritis.
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PMID:[Contribution of experimental pathology to the understanding of human pyelonephritis]. 837 12

Urinary levels of tissue inhibitor of metalloproteinase 1 (TIMP-1) higher than those of matrix metalloproteinase 9 (MMP-9) during acute pyelonephritis have previously been associated with a higher degree of acute inflammation and of postinfective renal scarring. The aim of the present study was to evaluate possible mechanisms by which TIMP-1 could affect the scarring process already during the acute phase of inflammation. The growth of Escherichia coli, bactericidal activity of fresh human blood, and respiratory burst, spontaneous apoptosis, and trans-basement membrane migration of normal human granulocytes were studied in vitro in the presence of different concentrations of recombinant human TIMP-1. To imitate the "normal" environment during inflammation in the kidney, granulocytes were also incubated with a conditioned medium from E. coli-stimulated renal epithelial cells. In order to compare our data with the in vivo situation, blood and urinary leukocyte levels were analyzed for 40 children with acute pyelonephritis, together with urinary MMP-9 and TIMP-1 levels. TIMP-1 at a concentration of 500 ng/ml increased the bactericidal activity of blood, increased the respiratory burst of granulocytes, decreased phosphatidylserine exposure and caspase 3 activity, which are features of spontaneous apoptosis, and inhibited granulocyte transmigration. Moreover, in the patients with pyelonephritis, MMP-9/TIMP-1 ratios in urine correlated with the degree of leukocyte transmigration. Thus, our data suggest that TIMP-1 specifically blocks the transmigration of granulocytes into urine. Entrapped and activated granulocytes, protected from apoptosis, might excessively destroy renal parenchyma and thus contribute to the pathogenesis of renal scarring following acute pyelonephritis.
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PMID:Tissue inhibitor of metalloproteinase 1 activates normal human granulocytes, protects them from apoptosis, and blocks their transmigration during inflammation. 1468 84

The aim of the research was to study blood responses to inflammatory processes in patients of different ages. The subjects of the study were 31 healthy persons and 198 patients, 116 of whom had pneumonia and 82 had chronic pyelonephritis. The patients were divided into three age groups: 16 to 39 years, 40 to 59 years, and older than 60 years. The following parameters were calculated on the basis of peripheral blood leukocyte composition and ESR: leukocyte intoxication index (LII), lymphocyte index (LymI), leukocyte shift index (LSI), leukocyte index (LI), leukocyte to ESR ratio index (LESRRI), lymphocyte-granulocyte index (LGI), total index (TI), neutrophile to lymphocyte ratio index (NLymRI), neutrophile to monocyte ratio index (NMRI), and lymphocyte to monocyte ratio index (LMRI). The majority of the indexes (LII, LymI, LSI, LI, LESRRI, LGI, and LMRI) in acute inflammation processes and some of them (LESRRI, NLymRI, and LMRI) in chronic inflammation altered significantly in all the age groups, which demonstrated that compensatory and adaptive mechanisms remained preserved in the elderly. The were age-dependent differences in blood responses to inflammation: LymI, LI, and LGI were significantly lower in the elderly with chronic pyelonephritis, whereas in Groups 1 and 2 there were no changes; NMRI was decreased in Groups 1 and 2 in chronic pyelonephritis and did not differ from the elderly controls. In acute inflammation, there were no significant differences from the controls in NlymRI in Group 3, while this parameter in Groups 1 and 2 differ from that in the controls. Thus, hematological indices make it possible to assess the work of effectory mechanisms of the immune system, the degree of their compensation in patients belonging to different age groups.
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PMID:[Peripheral blood responses in elderly patients with some prevalent diseases]. 1836 93

A 43-year-old woman was referred to our hospital for fever, general fatigue and left flank abdominal pain during the last two weeks. A blood test showed severe inflammation, and computed tomography (CT) study of the abdomen with intravenous contrast revealed swelling and irregular enhancement in the upper left kidney. Initially, we diagnosed it as xanthogranulomatous pyelonephritis and treated it with antibiotics. A percutaneous renal biopsy was performed because the white blood cell count remained elevated after the treatment. Histopathologic examination revealed a carcinoma. Therefore, we performed left nephroureterectomy. The diagnosis was high grade urothelial carcinoma of the renal pelvis, and it stained positive by immunohistochemical staining using anti-granulocyte-colony stimulating factor (G-CSF). The serum G-CSF level was also elevated on the same day. The patient received chemotherapy but, died 9 months after surgery. A G-CSF-producing urothelial carcinoma of the renal pelvis is known to have a poor prognosis in the Japanese literature. It is important to closely monitor a G-CSF producing tumor, when a patient shows severe inflammation, but no infection.
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PMID:[Granulocyte-colony stimulating factor-producing urothelial carcinoma of the renal pelvis : a case report]. 2382 67