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

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

The compromised host has recently increased because of the improvement of medical diagnosis and technology. Infection in the compromised host is somewhat different from that in common patients, since this infection is caused by impairment of the host defense mechanism. And the compromised host easily suffers from opportunistic infections. This situation prompted us to study the effect of biological response modifiers (BRMs), which activate the host defense mechanism against infections in the compromised host. We used streptozotocin (STZ)-induced diabetic mice, as experimental models of the compromised host. First, we investigated the bactericidal capacity of the perineal exudating neutrophils in diabetic mice, as one of the host defense mechanism. Second, we also studied the effect of Granulocyte-Colony Stimulating Factor (G-CSF) on diabetic mice with ascending pyelonephritis by P. aeruginosa. At 1 and 2 weeks after inducing the diabetic state, no difference was found in the bactericidal capacity of the perineal exudating neutrophils between normal mice and diabetic mice. At 3 weeks, however, this bactericidal capacity was markedly suppressed in these mice. This result suggested that a depression of host defense mechanisms in diabetics was caused by, in part, a suppression of bactericidal capacity of neutrophils. When G-CSF (2 micrograms/mouse) was injected subcutaneously once a day into diabetic mice, the suppression of the bactericidal capacity of neutrophils significantly recovered. We thus studied the effect of G-CSF on diabetic mice against infection. Diabetic mice increased their susceptibility to bacterial infection more than normal mice. In diabetic mice, administration of G-CSF (2 micrograms/mouse) yielded a lower incidence of infection and infection-induced mortality than those of controls. These data show that G-CSF may be of great value for prevention and treatment of opportunistic infections in the compromised host, especially in patients whose bactericidal capacity of neutrophils is depressed, as in diabetics.
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PMID:[Study of the prophylactic effect of human granulocyte-colony stimulating factor (G-CSF) on experimental pyelonephritis induced by Pseudomonas aeruginosa in diabetic mice]. 248 17

We investigated the prophylactic effect of Ubenimex 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 Ubenimex (100 micrograms/day/mouse) did not produce significant decreases of infection-induced mortality rate, but yielded a lower incidence of infection than of saline alone. Administration of Ubenimex was not able to increase the number of neutrophils during the experiment. An investigation of the bactericidal capacity of peritoneal exudating neutrophils revealed that Ubenimex prophylactic administration accelerated its capacity, although cyclophosphamide alone did not. These results suggest that Ubenimex has a prophylactic effect on bacterial infection in neutropenic mice, and that this effect, in part, depends upon the acceleration of bactericidal capacity of neutrophils produced by Ubenimex.
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PMID:[Study of the prophylactic effect of ubenimex on experimental pyelonephritis induced by Pseudomonas in neutropenic mice]. 251 30

A model of ascending unobstructed urinary tract infection (UTI) in mice was developed to study the significance of the antibiotic concentration in urine, serum, and kidney tissue for efficacy of treatment of UTI in general and pyelonephritis in particular. Outbred Ssc-CF1 female mice were used throughout the study, and Escherichia coli was used as the pathogen. The virulence of 11 uropathogenic E. coli isolates and 1 nonpathogenic laboratory E. coli strain was examined. Strain C175-94 achieved the highest counts in the kidneys, and this strain was subsequently used as the infecting organism. The model gave reproducible bladder infections, i.e., bacteria were recovered from 22 of 23 control mice after 3 days, and histological examination of kidney tissue showed that of 14 infected kidneys, 7 (50%) showed major histological changes, whereas 3 of 36 uninfected kidneys showed major histological changes (P = 0.018). Once the model was established, the efficacies of different doses of cefuroxime and gentamicin, corresponding to active concentrations in urine only or in urine, serum, and kidney tissue simultaneously, were examined. All cefuroxime doses resulted in significantly lower counts in urine than control treatments, but the dose which produced concentrations of cefuroxime only in urine and not in serum or kidney tissue had no effect on kidney infection. Even low doses of gentamicin (0.05 mg/mouse) resulted in concentrations in renal tissue for prolonged times due to accumulation. All gentamicin doses had a significant effect (compared to the effect of the control treatment) on bacterial counts in urine and kidneys. The antibiotic effect on bacterial counts in bladders was negligible for unknown reasons. Use of the mouse UTI model is feasible for study of the effect of an antibiotic in the urinary system, although the missing antibacterial effect in the bladder needs further evaluation.
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PMID:Development of a long-term ascending urinary tract infection mouse model for antibiotic treatment studies. 1060 38

Urinary tract infections (UTI) are among the most common bacterial infections of humans. The mouse provides an excellent and tractable model system for cystitis and pyelonephritis caused by Escherichia coli and other uropathogens. Using a well-established model of experimental cystitis in which the bladders of female mice are infected via transurethral catheterization, the molecular details of the pathogenesis of bacterial cystitis have been substantially illuminated in the last decade. Uropathogenic E. coli attach to bladder epithelium (both in human and mouse) via adhesive type 1 pili, establish a replicative niche within epithelial cell cytoplasm, and form intracellular bacterial communities that are protected from antibiotic effects and immune clearance. The use of different inbred and mutant mouse strains offers the opportunity to study outcomes of infection, including resolution, formation of quiescent intracellular bacterial reservoirs, chronic bacterial cystitis, and recurrent infections. Urine, bladder, and kidney tissues can be analyzed by bacterial culture, histology, immunohistochemistry, immunofluorescent and confocal microscopy, electron microscopy, and flow cytometry, while a broad array of soluble markers (e.g., cytokines) can also be profiled in serum, urine, and tissue homogenates by ELISA, Western blotting, multiplex bead array, and other approaches. This model promises to afford continued opportunity for discovery of pathogenic mechanisms and evaluation of therapeutic and preventive strategies for acute, chronic, and recurrent UTI.
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PMID:A Murine Model for Escherichia coli Urinary Tract Infection. 2646 8