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

Several virulence factors, such as O and K antigens and capacity to attach to uroepithelial cells, seem to be required for Escheria coli to cause acute pyelonephritis. These factors induce an immune response, however, which can modify the course and clinical expression of the infection. During acute pyelonephritis, autoantibodies to the Tamm-Horsfall protein increase. These antibodies, which probably are evoked by a cross-reaction noted between structures of E. coli LPS and the Tamm-Horsfall protein, may add to the renal tissue engagement in interstitial nephritis caused by bacterial pyelonephritis.
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PMID:Immunological aspects of pyelonephritis. 38 Aug 97

Purified lipopolysaccharide of Escherichia coli produced specific antibody when injected intraperitoneally or given to rats orally. Either route of immunization did not prevent ascending pyelonephritis in a diabetic rat model. The use of purified LPS excludes the potential contribution of other virulence factors of E. coli as protective antigens in the prevention of ascending pyelonephritis and confirms that anti-lipopolysaccharide antibody is not protective for ascending pyelonephritis.
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PMID:Lack of protection against ascending Escherichia coli pyelonephritis in diabetic rats following immunization with purified lipopolysaccharide. 354 11

In patients with recurrent pyelonephritis, the pathogenetic events proceed through intestinal colonization, spread to the urinary tract and persistence, seemingly uninterrupted by host defense mechanisms. The factors responsible for the deficient bacterial clearance from the kidneys of these patients, and the genetic control, have not been identified. The susceptibility to colonization has been linked to an increased receptivity for attaching bacteria of the uroepithelia, and to an overrepresentation of the P1 blood group phenotype. To evaluate the role of defects in host defense for the susceptibility to pyelonephritis, experimental UTI in mouse strains with known deficiencies was used. A highly significant increase in susceptibility was noted for C3H/HeJ compared to C3H/HeN mice. The bacterial recovery was inversely correlated to the mitogenic response to LPS. Back-cross analysis revealed a linkage of susceptibility to the Lpsd/Lpsd genotype. In contrast, T and B lymphocyte and complement (C5) defects had little effect on the clearance of Escherichia coli from the kidneys. It is concluded that the inflammatory mechanisms induced by LPS are essential for resistance to experimental pyelonephritis.
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PMID:Genetic factors in host resistance to urinary tract infection. 393 16

In patients with recurrent pyelonephritis, the pathogenetic events proceed through intestinal colonization, spread to the urinary tract and persistence, seemingly uninterrupted by host defense mechanisms. The factors responsible for the deficient bacterial clearence from the kidneys of these patients, and the genetic control, have not been identified. The susceptibility to colonization has been linked to an increased receptivity for attaching bacteria of the uroepithelia, and to an overrepresentation of the P1 blood group phenotype. To evaluate the role of defects in host defense for the susceptibility to pyelonephritis, experimental UTI in mouse strains with known deficiencies was used. A highly significant increase in susceptibility was noted for C3H/HeJ compared to C3H/HeN mice. The bacterial recovery was inversely correlated to the mitogenic response to LPS. Back-cross analysis revealed a linkage of susceptibility to the Lpsd/Lpsd genotype. In contrast, T and B lymphocyte and complement (C5) defects had little effect on the clearance of Escherichia coli from the kidneys. It is concluded that the inflammatory mechanisms induced by LPS are essential for resistance to experimental pyelonephritis.
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PMID:Genetic factors in host resistance to urinary tract infection. 637 64

Tubulointerstitial and periglomerular inflammation and fibrosis are important consequences of pyelonephritis. The pathogenesis of these abnormalities is not fully understood. Renal tubular epithelial cells (RTEC) elaborate biologically active materials following incubation with bacteria. Nitric oxide (NO) is an inflammatory mediator and it modulates the accumulation of extracellular matrix proteins. Therefore, we studied whether RTEC-E. coli interaction products regulate NO production by cultured rat renal medullary interstitial cells (RMIC) and mesangial cells (MC). RMIC and MC were maintained in media containing IFN-gamma and LPS for 24-72 h. Test media contained either no further additives or 20% supernatants from RTEC incubated with E. coli or bacterial cell products. RTEC-E. coli interaction products significantly increased NO production in RMIC and MC. This stimulation in NO production was not associated with changes in inducible nitric oxide synthase (iNOS) gene or protein expression. These findings indicate that RTEC-E. coli interaction products increase NO production in RMIC and MC by directly stimulating iNOS enzymatic activity. Altered NO production by renal cells may contribute to tubulointerstitial inflammation in acute and chronic pyelonephritis.
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PMID:Renal tubular epithelial cell-E. coli interaction products stimulate nitric oxide production in cultured rat renal medullary interstitial and mesangial cells. 902 69

It has been shown that in patients with acute pyelonephritis a spontaneous production of the interleukin IL-1 remains unchanged, while that stimulated with the aid of LPS is significantly below the norm. A spontaneous secretion of IL-2 in patients with chronic pyelonephritis has also been found unchanged, whereas in acute pyelonephritis this same parameter tends to rise above the level recordable in healthy donors. The production of this lymphokine stimulated with the aid of PhHA is significantly lower both in acute and chronic pyelonephritis. The level of cells carrying receptors to IL-2 is appreciably above the norm in patients with acute pyelonephritis, whereas in those presenting with the chronic process this parameter does not differ from that in the control group. The data obtained suggest distinctive features in the interleukin link of immunity (IL-1, IL-1, IL-2P) in patients with pyelonephritis.
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PMID:[The level of interleukins (IL-1 and IL-2) and of IL-2R+ cells in patients with acute and chronic pyelonephritis]. 979 14

It has been suggested that treatment of systemic infections caused by Gram-negative bacteria with beta-lactam agents might add to the inflammatory process by resulting in the release of endotoxins (LPS) upon death of the Gram-negative bacteria. To evaluate that hypothesis, 25 patients with acute pyelonephritis of Gram-negative aetiology were given intravenous cefuroxime 1.5 g tid. Blood samples were collected at various time intervals for blood culture and for the determination of LPS, tumour necrosis factor-alpha (TNFalpha) and cefuroxime levels. LPS remained elevated at levels equal to those before the administration of cefuroxime over the first 24 h of therapy. A positive correlation was detected between LPS and drug levels 6 h after the initiation of therapy. Fever persisted in 50, 37.5 and 16.7% of patients 48, 72 and 96 h after the start of treatment, respectively, followed by a rise of LPS at levels above the baseline. Blood cultures taken at the same time were sterile. A wide range of TNFalpha levels were found at similar times of sampling, indicating that LPS triggers considerable TNFalpha production in the serum of some patients but not in others. It is concluded that antibiotic-induced endotoxaemia is a phenomenon that might be observed in patients receiving cefuroxime and that might be responsible for the persistence of fever despite negative blood cultures.
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PMID:Impact of cefuroxime administration on endotoxin (LPS) and tumour necrosis factor-alpha (TNFalpha) blood levels in patients suffering from acute pyelonephritis: a preliminary report. 1022 14

Pyelonephritis, in which renal tubular epithelial cells are directly exposed to bacterial component, is a major predisposing cause of renal insufficiency. Although previous studies have suggested C-C chemokines are involved in the pathogenesis, the exact source and mechanisms of the chemokine secretion remain ambiguous. In this study, we evaluated the involvement of Toll-like receptors (TLRs) in C-C chemokine production by mouse primary renal tubular epithelial cells (MTECs). MTECs constitutively expressed mRNA for TLR1, 2, 3, 4, and 6, but not for TLR5 or 9. MTECs also expressed MD-2, CD14, myeloid differentiation factor 88, and Toll receptor-IL-1R domain-containing adapter protein/myeloid differentiation factor 88-adapter-like. Synthetic lipid A and lipoprotein induced monocyte chemoattractant protein 1 (MCP-1) and RANTES production in MTECs, which strictly depend on TLR4 and TLR2, respectively. In contrast, MTECs were refractory to CpG-oligodeoxynucleotide in chemokine production, consistently with the absence of TLR9. LPS-mediated MCP-1 and RANTES production in MTECs was abolished by NF-kappaB inhibition, but unaffected by extracellular signal-regulated kinase inhibition. In LPS-stimulated MTECs, inhibition of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase significantly decreased RANTES, but did not affect MCP-1 mRNA induction. Thus, MTECs have a distinct expression pattern of TLR and secrete C-C chemokines in response to direct stimulation with a set of bacterial components.
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PMID:Roles of toll-like receptors in C-C chemokine production by renal tubular epithelial cells. 1216 29

Toll-like receptors (TLR) are an emerging family of receptors that recognize pathogen-associated molecular patterns and promote the activation of leukocytes and intrinsic renal cells. Ligands of the TLR include exogenous microbial components such as LPS (TLR4), lipoproteins and peptidoglycans (TLR1, -2, -6), viral RNA (TLR3), bacterial and viral unmethylated cytosin-guanosin dinucleotide (CpG)-DNA (TLR9), and endogenous molecules including heat-shock proteins and extracellular matrix molecules. Upon stimulation, TLR induce expression of inflammatory cytokines or costimulatory molecules via the MyD88-dependent and MyD88-independent signaling pathways shared with the interleukin-1 receptors. TLR are differentially expressed on leukocyte subsets and non-immune cells and appear to regulate important aspects of innate and adaptive immune responses. Tubular epithelial cells are among the non-immune cells that express TLR1, -2, -3, -4, and -6, suggesting that these TLR might contribute to the activation of immune responses in tubulointerstitial injury (e.g., bacterial pyelonephritis, sepsis, and transplant nephropathy). In addition, TLR9 has been shown to be involved in antigen-induced immune complex glomerulonephritis and lupus nephritis by regulating humoral and cellular immune responses. TLR are evolutionary conserved regulators of innate and adaptive immune responses. It is likely that TLR are involved in many if not all types of renal inflammation. Here the authors provide an overview on the biology of TLR, summarize the present data on their expression in the kidney, and provide an outlook for the potential roles of TLR in kidney disease.
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PMID:Signaling danger: toll-like receptors and their potential roles in kidney disease. 1503 87

To assess the efficacy of clarithromycin as an immunomodulator in experimental sepsis with Escherichia coli, acute pyelonephritis was induced after ligation of the right ureter and injection of the test isolate into the renal pelvis in 40 rabbits. Four groups of treatment were applied with administration of therapy on advent of sepsis-associated pulmonary oedema, as follows: A: controls; B: clarithromycin; C: amikacin, D: both agents. Survival was recorded along with estimation of serum levels of endotoxins (LPS), of tumour necrosis factor-alpha (TNFalpha), malondialdehyde (MDA) and of bacterial counts. Mean survival of groups A, B, C and D was 2.51, 7.60, 10.25 and 11.40 days, respectively. Serum levels of TNFalpha and of MDA of group A increased over-time. Pulmonary oedema at 6 h after bacterial challenge was accompanied by increase of TNFalpha and MDA; administration of clarithromycin decreased their values. It is concluded that intravenous clarithromycin might constitute a promising immunomodulatory agent for the management of sepsis since its efficacy was proved after administration on presentation of sepsis-associated pulmonary oedema. The presented findings emphasise the need for further clinical research of the use of clarithromycin for the therapy of Gram-negative sepsis.
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PMID:Clarithromycin co-administered with amikacin attenuates systemic inflammation in experimental sepsis with Escherichia coli. 1566 88


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