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)

Urinary tract infections caused by Escherichia coli are associated with a local and systemic antibody response. We have studied the serum and urine antibody responses to Escherichia coli in men and women with pyelonephritis, cystitis, and asymptomatic bacteriuria. Protein immunoblots consistently demonstrated serum antibody response to lipopolysaccharide (LPS). Anti-LPS antibody titres rose significantly and progressively when comparing acute with convalescent sera in those who have had their first urinary infection. For those with repeated infections, high titre LPS antibodies were present and did not change significantly between acute and convalescent sera. Antibody responses to the major outer membrane proteins were present but did not differ significantly when compared with normal human serum. A specific anti-P pilus antibody response was demonstrated by immunoblotting. Anti-P pilus antibody was quantitated using ELISA and the titres were found to be very low. Three other techniques were also used to demonstrate the presence of serum antibody. Antibody was detectable by immunofluorescence, but the antigenic specificity of the antibody was more difficult to ascertain. Immunoprecipitation was more specific for determining the nature of the antibody response. Lastly, immunoelectron microscopy was valuable in demonstrating antipilus and antiflagellar antibodies. Immunoelectron microscopy and immunoblotting provided evidence that human antiserum to P pili was modestly cross-reactive and could bind heterologous P pili. These studies indicated that the major antibody response in humans occurs after pyelonephritis and is directed against LPS. An anti-P pilus response is frequently present and is cross-reactive to some extent with other P pili.
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PMID:The human antibody response to uropathogenic Escherichia coli: a review. 304 23

We used immunoblotting to examine the serologic antibody responses to outer membrane proteins (OMP) of Escherichia coli in both symptomatic and asymptomatic elderly subjects with urinary tract infections. Controls with no present or past urinary tract infections showed variable weak immunoglobulin G (IgG) antibodies to OMP of infecting strains. Elderly individuals with asymptomatic infections demonstrated antibody to both lipopolysaccharide (LPS) and OMP of their infecting strain, with consistent cross-reactivity to OMP of other infecting strains. Young females with acute pyelonephritis showed an IgG response to LPS and OMP with cross-reactivity to OMP of other strains. Elderly individuals with symptomatic invasive infections had strong reactions to both LPS and OMP in specimens collected during the acute phase, generally with an increase in intensity in specimens from convalescent patients. They also demonstrated extensive cross-reactivity to LPS and OMP from all other infecting strains. IgM antibody was not observed in any patients. These data confirm other reports of low levels of antibodies to OMP of E. coli in normal populations. Asymptomatic bacteriuria in this population is associated with antibody responses to the LPS and OMP of the infecting strain. Elderly individuals with invasive infections had initial reactions to the infecting strain with an apparent increase in intensity during convalescence. Antibodies to the major OMP appear to be broadly cross-reactive.
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PMID:Immunoblot analysis of serologic response to outer membrane proteins of Escherichia coli in elderly individuals with urinary tract infections. 305 63

The last decade has provided new insight into the mechanisms of host-parasite interactions in the urinary tract. Reduction of host resistance appears to reduce the requirement for bacterial virulence, whereas the resistant host becomes infected with bacteria of high virulence. In the resistant host, bacterial virulence can be defined as the sum of properties required to colonize the urinary tract and induce tissue reactions. The ability to attach to uroepithelial cells is the single property most frequently associated with pyelonephritogenic clones. Attachment to the Gal alpha 1-4Gal beta-containing receptors promotes localization of bacteria to the kidney and the induction of lipopolysaccharide-mediated inflammation. Other virulence factors, defined by increased frequency in acute pyelonephritis compared with asymptomatic bacteriuria, include haemolysin and aerobactin production. Among the factors which influence the natural resistance to urinary tract infection are urinary flow and reactivity to endotoxin. The resistance induced by natural exposure to infection or immunization may be protective in experimental models, but the importance of this is not yet defined. The localization, severity and sequelae of urinary tract infection are determined by the balance between bacterial virulence and host resistance. Although disease is a result of the interaction between bacterial virulence and host resistance, these components are discussed separately for clarity.
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PMID:Host parasite interaction in urinary tract infection. 315 43

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

The relative contributions of host resistance and bacterial virulence were analyzed in a mouse model for ascending urinary tract infection. The congenic mouse strains C3H/HeJ and C3H/HeN were used in parallel. They differ in their reactivity to lipopolysaccharide (LPS) and susceptibility to experimental urinary tract infection. C3H/HeJ cells are susceptible to infection and are nonresponders to LPS (Lpsd Lpsd), whereas C3H/HeN cells respond to LPS and are resistant to infection (Lpsn Lpsn). The Escherichia coli pyelonephritis isolate GR-12, serotype O75K5, expressing adhesins specific for globoseries glycolipids (P fimbriae) and for mannosides (type-1 fimbriae), and its derivatives deficient in these factors were used, either singly or in combination, to establish experimental infections. In C3H/HeN mice, the relative persistence of E. coli was inversely proportional to its phagocytosis in vitro. Loss of the O75 and K5 antigens increased the tendency toward hydrophobic interaction, promoted phagocytosis, and reduced persistence in the kidneys. This was not the case in C3H/HeJ mice, in which O75- and K5- serotypes persisted in the same extent as did the parent strain. The total number of bacteria recovered from the kidneys of C3H/HeJ mice was about 1,000-fold higher than the number recovered from kidneys of C3H/HeN mice 24 h after infection. Previous studies have demonstrated a delayed influx of polymorphonuclear leukocytes into the urinary tracts of C3H/HeJ mice. The results are consistent with the hypothesis that phagocyte activation through LPS is a major defense mechanism against E. coli in the kidney, a property in which C3H/HeJ mice are deficient.
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PMID:Bacterial virulence versus host resistance in the urinary tracts of mice. 355 94

Vaccination with heat-killed or formalinized cells of E coli 0:111, or E coli 06 (Williams), prevented retrograde E coli pyelonephritis. Since there was no bacteremia and no urinary antibody, the vaccination appeared to protect by immune reactions operating in the kidney itself. The vaccine failed to protect against a highly virulent form of E coli 06 (Riffle), possibly because the amount of antibody to its lipopolysaccharide was inadequate. Since all three strains possessed K antigen in approximately equal amounts, the difference in results was not attributed to its presence.
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PMID:Immunization against retrograde pyelonephritis. II. Prevention of retrograde Escherichia coli pyelonephritis with vaccines. 459 Jun 46

The local immune response to pili of Escherichia coli O6:K13:H1 was determined in experimental hematogenous pyelonephritis in rabbits. Pili purified from sheared cells by ammonium sulfate precipitation were found to be pure by electron microscopy and negative for lipopolysaccharide by limulus lysate assay. Antipilus antibody was detected in serum and newly synthesized protein from infected animals with enzyme-linked immunosorbent assay. Serum and local (intrarenal) antibodies were of the immunoglobulin G class, were detectable by day 20 of infection, and persisted though 250 days of infection. These data suggest that pili are present on the organism at the site of infection, since they induce the local synthesis of antipilus antibody in experimental pyelonephritis.
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PMID:Local immune response to Escherichia coli pili in experimental pyelonephritis. 611 36

Escherichia coli strains isolated from three groups of patients with urinary tract infections, such as acute pyelonephritis, acute cystitis, and asymptomatic bacteriuria, were analyzed with respect to their physicochemical surface properties by means of polymer two-phase partitioning in dextran-polyethylene glycol systems and hydrophobic interaction chromatography on Octyl-Sepharose. Strains causing acute pyelonephritis constituted a homogenous group which, depending on the growth conditions, demonstrated smooth-type lipopolysaccharide, elevated negative charge, and liability to hydrophobic interaction, whereas strains isolated from acute cystitis and asymptomatic bacteriuria showed a more heterogenous pattern.
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PMID:Physicochemical surface properties of Escherichia coli strains isolated from different types of urinary tract infections. 611 38

Epidemiological data show that O18:K1 Escherichia coli is a common cause of neonatal bacteremia and meningitis. These bacteria were capable of multiplying in the bloodstream of newborn rats and were resistant to the bactericidal effects of complement in the absence of specific antibodies. The roles played by the O antigen and the K antigen in complement resistance were analyzed by comparing the bactericidal effects of normal sera and of sera deficient in various complement components or in immunoglobulins. These sera were tested on O18:K1 bacteria and on mutants lacking either the lipopolysaccharide O antigen or the K1 capsular polysaccharide. In addition, O1:K1 cells, which can cause pyelonephritis but which are rare in newborn meningitis and which do not multiply in the bloodstream of newborn rats, were also examined. Different mechanisms of protection against the alternative and classical pathways were recognized: K1-positive cells were resistant to the bactericidal activity of sera deficient in classical complement pathway components, whereas K1-negative cells were sensitive to these sera. Based on these results and on those from complement fixation assays, the K1 sialic acid polysaccharide impedes the activation of, and thus protects the bacteria against, the alternative complement pathway. Not only the K1-negative mutant cells but also O1:K1 bacteria and mutants lacking the O18 oligosaccharide repeating units of the lipopolysaccharide were sensitive to the classical complement pathway. These bactericidal effects were observed even in the absence of specific antibodies. It is proposed that both the K1 capsule and the O18 oligosaccharide restrict antibody-independent classical pathway activation by shielding deeper structures on the cell membrane that are capable of activating this pathway.
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PMID:Role of the capsule and the O antigen in resistance of O18:K1 Escherichia coli to complement-mediated killing. 619 96

Injection of heat killed bacteria into kidney parenchyma results in pathologic lesions similar to chronic pyelonephritis while immunosuppression reverses this phenomenon. These observations and the propensity of lipid A to bind to cell membranes suggest that the lipid component of bacterial lipopolysaccharide antigens may be important in the pathogenesis of kidney tubule cell death. The right kidneys of syngeneic Fischer 344 rats were repeatedly injected with glycolipid prepared from Salmonella minnesota Re 595 cell walls. As a control, the contralateral kidney was injected with normal saline. The inflammatory response observed in the glycolipid injected kidney was significantly greater (p less than 0.005) than the response detected in the contralateral saline injected control kidney. Electron microscopy of kidney tubule cells incubated with peroxidase conjugated glycolipid demonstrated glycolipid bound to the kidney tubule cell plasma membranes. These studies suggest that individual antigenic components can induce kidney lesions and tubule cell death similar to that seen in chronic pyelonephritis.
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PMID:Salmonella Minnesota Re 595 lipid A induced nephritis. 706 6


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