Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0519030 (Klebsiella)
 21,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order for a urinary tract infection to begin, the pathogenic bacteria must first adhere to the urothelial surface. An in vivo method for quantitation of bacterial adherence to urothelium has been developed. Immunization by instillation of bacterial antigens into the rat bladder decreased bacterial adherence. Bladder immunization was more effective than subcutaneous immunization. Preinfection by Escherichia coli decreased subsequent adherence of Klebsiella pneumoniae. Increasing antiadherence factors may offer a new approach to the treatment of recurrent urinary tract infections.
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PMID:Effect of immunization of bacterial adherence to urothelium. 36 28

The possible role of pili in the pathogenesis of urinary tract infection caused by Klebsiella pneumoniae was investigated in a rat model of cystitis by utilizing piliated- and nonpiliated-phase organisms derived from a single parent strain. Bladder surfaces were examined for evidence of infection by scanning electron microscopy. In animals infected with piliated-phase organisms, foci of infection were evident in the majority of bladders examined. Rat bladders associated with nonpiliated-phase bacteria showed little evidence of infection. The ability of methyl-D-mannoside, a known inhibitor of pilus-mediated adherence to mammalian cells, to protect the bladder surface from colonization was also tested. The results showed a significant decrease in the ability of piliated-phase K. pneumoniae to establish infection in bladders. These observations suggest that pili may play an integral role in the ability of K. pneumoniae to cause urinary tract infections by mediating the attachment of the bacteria to the uroepithelial surface.
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PMID:Effect of piliation on Klebsiella pneumoniae infection in rat bladders. 610 91

Klebsiella pneumoniae is an important cause of urinary tract infection (UTI), but little is known about its pathogenesis in vivo. The pathogenesis of the K. pneumoniae cystitis isolate TOP52 was compared to that of the uropathogenic Escherichia coli (UPEC) isolate UTI89 in a murine cystitis model. Bladder and kidney titers of TOP52 were lower than those of UTI89 at early time points but similar at later time points. TOP52, like UTI89, formed biofilm-like intracellular bacterial communities (IBCs) within the murine bladder, albeit at significantly lower levels than UTI89. Additionally, filamentation of TOP52 was observed, a process critical for UTI89 evasion of neutrophil phagocytosis and persistence in the bladder. Thus, the IBC pathway is not specific to UPEC alone. We investigated if differences in type 1 pilus expression may explain TOP52's early defect in vivo. The type 1 pilus operon is controlled by recombinase-mediated (fimE, fimB, and fimX) phase variation of an invertible promoter element. We found that K. pneumoniae carries an extra gene of unknown function at the 3' end of its type 1 operon, fimK, and the genome lacks the recombinase fimX. A deletion mutant of fimK was constructed, and TOP52 Delta fimK had higher titers and formed more IBCs in the murine cystitis model than wild type. The loss of fimK or expression of E. coli fimX from a plasmid in TOP52 resulted in a larger phase-ON population and higher expression levels of type 1 pili and gave TOP52 the ability to form type 1-dependent biofilms. Complementation with pfimK decreased type 1 pilus expression and biofilm formation of TOP52 Delta fimK and decreased UTI89 biofilm formation. Thus, K. pneumoniae appears programmed for minimal expression of type 1 pili, which may explain, in part, why K. pneumoniae is a less prevalent etiologic agent of UTI than UPEC.
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PMID:Utilization of an intracellular bacterial community pathway in Klebsiella pneumoniae urinary tract infection and the effects of FimK on type 1 pilus expression. 1841 Dec 85