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)

We studied the susceptibility of Enterobacteriaceae to four aminoglycosides (gentamicin, tobramycin, netilmicin et amikacin). We determined their phenotypes of resistance by taking into account both the critic concentrations of the CFA (french committee for antibiogram) and the MIC of the main susceptible population of each species. The most frequent phenotypes were GTNt, TNtA and GTNtA. Amikacin resistance including phenotypes were essentially found in Klebsiella and Serratia (35% and 53% of the strains, respectively); with respect to amikacin, the phenotype expression may be insufficient to exceed the sensitive critic concentration of the CFA. Amikacin resistant strains were isolated from chronically infected patients with devices, such as urinary catheters or tracheal cannula. These results suggest a strains or plasmids outbreak.
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PMID:[Current status of aminoglycoside resistance in hospital Enterobacteriaceae]. 304 39

We studied the colonization-factor antigen I (CFA/I) fimbriae- and heat-stable enterotoxin (ST)-coding plasmid of enterotoxigenic Escherichia coli (strain H10407, serotype O78:H11) pathogenic for humans. With use of conjugal-transfer system of E. coli H10407 and transposon-labeling techniques, the virulence plasmid was shown to be transferable to many species of the family Enterobacteriaceae, including the enteropathogens, Shigella and Salmonella species, and the opportunistic pathogens, Klebsiella, Enterobacter, Citrobacter, Edwardsiella, Serratia, and Proteus species. The virulence plasmid-carrying transconjugants produced both CFA/I fimbriae and ST (exotoxin). Moreover, most of the transconjugants stably inherited the virulence plasmid, although plasmid stability was greatly dependent on culture temperature. Finally, administration of the virulence plasmid-carrying living bacterial cells of Klebsiella, Enterobacter, and Citrobacter species and E. coli K12 resulted in fluid accumulation in both infant-mouse and rabbit ileal-loop tests.
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PMID:A virulence plasmid in Escherichia coli enterotoxigenic for humans: intergenetic transfer and expression. 614 47

The L1 protein occurs at high concentrations in neutrophils, monocytes, certain reactive tissue macrophages, squamous mucosal epithelia, and reactive epidermis. It constitutes in fact about 60% of the neutrophilic cytosol protein fraction. The two L1 chains (L1H and L1L) are referred to by a bewildering collection of names, various authors having different preferences (MRP-8 and MRP-14; CFA or calgranulin A and B). The most recent proposal is calprotectin because of its calcium-binding properties and antimicrobial effect shown in vitro. L1 belongs to the S-100 protein family and may be involved in the regulation of keratinocyte proliferation and differentiation. It exists at high levels in blood and interstitial tissue fluid in several infectious, inflammatory, and malignant disorders, and it is released abundantly in foci of granulocytes and macrophages. The C-terminal sequence of the L1H chain has been shown to be identical to the N-terminus of peptides known as neutrophil immobilizing factors. Such an activity of L1 could be important for the accumulation of vital granulocytes, while L1 released from neutrophils, macrophages and epithelial cells might exert antimicrobial activity, perhaps by depriving microorganisms of zinc. The minimum inhibitory concentrations of L1 in vitro were found to be 4-32 mg/l for Candida albicans, 64 mg/l for Staphylococcus aureus, 64-256 mg/l for S. epidermidis, and 256 mg/ml for Escherichia coli and Klebsiella spp. Killing was observed at 2-4 times higher concentrations. In patients with HIV infection, those who developed oral candidiasis had significantly lower parotid L1 levels than those who did not (67 micrograms/l vs. 216 micrograms/l).
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PMID:The leucocyte protein L1 (calprotectin): a putative nonspecific defence factor at epithelial surfaces. 852 6

Longus is a long pilus produced by human enterotoxigenic Escherichia coli (ETEC) which shares significant structural and biochemical features with class-B type-4 pili. These pili include the toxin-coregulated pilus (TCP) of Vibrio cholerae, the bundle-forming pilus (BFP) of enteropathogenic E. coli and both longus and the colonization factor antigen III (CFA/III) of ETEC. These pili are produced under defined growth conditions indicating that they are under the control of different regulatory elements. While TCP is chromosomally encoded, the remaining pili are encoded on large virulence plasmids. Longus and CFA/III are closely related pili although certain DNA and protein differences also exist between them. This may account for the differences in the regulation, surface presentation, antigenicity, and prevalence of these two pilins among ETEC. Neighboring lngA, a second open reading frame termed lngB was found which encodes a protein with significant homology to proteins which are part of a type-II secretory system such as XcpV, OutC, and PulO of Pseudomonas aeruginosa, Erwinia chrysanthemi, and Klebsiella pneumoniae, respectively. This suggests that lngB may be an accessory gene involved in biogenesis of longus.
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PMID:Longus pilus of enterotoxigenic Escherichia coli and its relatedness to other type-4 pili--a minireview. 922 72

We investigated whether oral administration of LPS exacerbated collagen-induced arthritis (CIA) in mice, which was an experimental model of autoimmune disease. CIA was induced by s.c. injection of type II collagen emulsified with CFA into the base of the tail (day 0) followed by a booster injection on day 21. To examine the ability of LPS to exacerbate CIA, varying doses of LPS were orally administered on day 50. The results showed that administration of LPS was followed by reactivation of CIA in a dose-related fashion. Histologically, on day 55 there were marked edema of synovium proliferated by day 50, new formation of fibrin, and intense infiltration of neutrophils accompanied with a large number of mononuclear cells. Severe destruction of cartilage and subchondral bone was also observed on day 70. The reactivation of CIA by oral administration of LPS was associated with increase in anti-type II collagen IgG and IgG2a Abs as well as varying kinds of cytokines including IL-12, IFN-gamma, IL-1beta, and TNF-alpha. Polymyxin B sulfate given either orally or i.v. suppressed the recurrence of CIA. Increased amounts of LPS were found in sera of mice given the endotoxin orally. LPS from Salmonella enteritidis, Salmonella typhimurium, and Klebsiella pneumoniae and its component, lipid A from Escherichia coli, also reactivated the disease. These findings suggest that LPS from intestinal bacteria may play a role in the exacerbation of autoimmune joint inflammation.
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PMID:Oral administration of lipopolysaccharide exacerbates collagen-induced arthritis in mice. 1047 13