Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The capsular polysaccharide complex (CPC) of Bacteroides fragilis exhibits unusual biological properties. This polysaccharide complex promotes the formation of intraabdominal abscesses and, when administered systemically, can prevent abscess induction in a rat model of intraabdominal sepsis. Each of these biological properties is mediated by a T cell-dependent immune mechanism. The CPC consists of two distinct polysaccharides, PS A and PS B, each with repeating units that have positively charged amino groups and negatively charge carboxyl or phosphate groups. Analysis of these polysaccharides as well as of other charged polysaccharides of bacterial origin, before and after chemical modification, revealed that the oppositely charged groups are required for promotion of intraabdominal abscesses as well as for the distinct properties associated with the B. fragilis CPC and delineate one mechanism by which these biological responses occur.
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PMID:Structure and function of Bacteroides fragilis capsular polysaccharides: relationship to induction and prevention of abscesses. 754 35

We used transposon (TnphoA) mutagenesis to study the role of virulence factors of pathogenic Escherichia coli strains associated with septicemia in calves and piglets. We have produced an avirulent and serum-sensitive mutant of wild-type pathogenic strain 5131 O115:K"V165":F165 and have localized and identified the TnphoA insertion in the pstC gene of the pst-phoU operon. This operon encodes the PstSCAB transporter and PhoU protein that negatively regulate the phosphate (Pho) regulon. This mutation is pleiotropic and could have an effect on pathogenicity and on the production of the surface polysaccharides of strain 5131. The mutant demonstrated restored repressibility of alkaline phosphatase and regained the capacity to resist serum and to survive systemically for at least 5 days in experimentally inoculated pigs when complemented with plasmid pAN92, bearing the pst-phoU operon.
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PMID:Identification of a mutation in the pst-phoU operon that reduces pathogenicity of an Escherichia coli strain causing septicemia in pigs. 759 Nov 58

Struvite renal stones are caused by infection of the urine with bacteria that synthesize the enzyme urease. Ammonium is released by the breakdown of urea by urease, the urine becomes highly alkaline, and magnesium ammonium phosphate (struvite) and carbonate apatite crystallize. Incorporation of the infecting bacteria within the developing stone, results in a focus of infection that is resistant to conventional antimicrobial therapy, and which is manifested clinically by repeated urinary tract infection caused by persistent bacteriuria. Extracorporeal shock wave lithotripsy (ESWL) currently is accepted as the election treatment for most renal calculi. This trial examines the bacteriologic aspects pre and post-ESWL. Eighty adult patients, 47 females and 33 males, without clinical signs of urinary tract infections (UTI) were submitted to urine cultures pre and post-ESWL. The first 50 patients underwent during and post-ESWL, 150 blood cultures, which all proved to be negative, confirming very low risk of generalized sepsis. No patient presented fever, chills or rigors pre or postprocedures. With respect to urine cultures 43 patients (52.5%) had a pre-ESWL UTI, in comparison to 49 (60%) who had a UTI post-ESWL. The distribution of organisms pre and post-ESWL was as follows: Proteus mirabilis (22/22), Escherichia coli (11/11), Pseudomonas aeruginosa (4/5), Klebsiella pneumoniae (2/2), Enterobacter cloacae (0/1), Alcaligenes odorans (1/2) Enterococcus faecalis (1/3), Staphylococcus saprophyticus (1/2) and Candida albicans (1/1). In this study 6 patients presented bacteriuria post-ESWL probably due to bacteria from inside the calculi. According to these results, the risk of bacteremia seems to be very low. In 60% of staghorn renal stones we could demonstrate a bacterial infection.
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PMID:[Staghorn renal lithiasis treated with shock waves. Bacteriologic aspects]. 765 75

The binding properties and specificity of the SdJ5-1.17.15 (SdJ5) human IgM monoclonal antibody (mAb), prepared against S. minnesota R595 heat killed whole organisms, were assessed by dot blot assay in vitro. In that assay, lipopolysaccharide (LPS) related antigens, immobilized on nitrocellulose membrane, were reacted with the test and control human IgM antibodies. Results indicated that SdJ5 mAb reacted specifically with lipid A, a component of LPS, from a variety of bacterial species, but not with the whole LPS molecule. The inability of the mAb to react with whole LPS in dot blot assay was attributed to the possible effect of the solid phase on epitope exposure or structure. This hypothesis was tested by inhibition studies which indicated that liquid phase adsorption with LPS abolished or greatly reduced the specific recognition of solid phase lipid A by the mAb. These results indicated that LPS-associated antigens were recognized by the SdJ5 anti-lipid A mAb in liquid, but not solid, phase. In an attempt to identify the SdJ5-specific epitope on lipid A, the pattern of reactivities of different lipid A analogues with the mAb were examined by dot blot assay. Results indicated that a combination of the fatty acid side chains and the phosphate groups of lipid A (both groups being implicated as important for sepsis mediation) were either directly involved in the epitope structure or affected the exposure of epitope in solid phase. Because SdJ5 recognizes an LPS epitope on lipid A closely associated with endotoxin activity, this mAb could potentially be a useful therapeutic agent against septic shock.
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PMID:Lipopolysaccharide epitope specificity and binding cross reactivity of the human IgM anti-lipid A monoclonal antibody SdJ5-1.17.15. 768 72

The effect of heparan sulfate (HS) on survival rate, bacterial translocation, and host defense was studied in a model of gut-derived sepsis that included transfusion-induced immunosuppression. Balb/c mice were treated pre- and postburn injury and bacterial challenge with HS, 5 mg/kg/day, or sterile phosphate-buffered saline. The HS pre- and postburn treated animals showed a significant improvement in survival compared to control animals (80 vs. 30%, p = .004, and 60 vs. 20%, p = .02, respectively). A lower amount of translocation was observed in the spleen (p < or = .001) of the HS group compared to control group. Quantitative colony counts and the calculated percentage of viable bacteria showed that the ability to kill translocated organisms was enhanced in all tissues of the animals receiving HS. These data suggest that treatment with HS positively affects the outcome in gut-derived sepsis. The beneficial effect was related both to an improved gut barrier function and to an enhanced host defense.
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PMID:Heparan sulfate increases survival during gut-derived sepsis by decreasing bacterial translocation and enhancing host defense. 775 15

Monophosphoryl lipid A (MPL) is a less toxic derivative of lipid A that enhances survival from endotoxemia. This study examined whether MPL induced resistance to Gram-positive sepsis and cytokines. Mice were administered MPL or saline (phosphate-buffered saline) and challenged 24 h later with live Staphylococcus aureus (SA), staphylococcus enterotoxin B (SEB), toxic shock syndrome toxin (TSST-1), and tumor necrosis factor (TNF). Survival was determined at 72 h. A separate set of animals was phlebotomized for determination of cytokines. MPL increased survival from S. aureus bacteremia from 20 to 87% (p < .05). Interleukin-6 (IL-6) and interleukin-1 (IL-1) and TNF were also significantly decreased. SEB and TSST survival were enhanced from 10 to 90% (p < .05). In SEB-treated animals, TNF and IL-6 levels were significantly decreased. Survival from TNF infusion was increased from 20 to 100% with MPL, however, no significant differences in cytokines were observed. These data suggest that MPL induces resistance to Gram-positive sepsis and cytokine-mediated activity.
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PMID:Monophosphoryl lipid A protects against gram-positive sepsis and tumor necrosis factor. 775 20

Experimental data suggest an association between hypomagnesaemia and hypokalaemia, and also with hypophosphataemia, but there have been few large studies using clinical results to study the prevalence of hypophosphataemia and/or hypokalaemia in patients with hypomagnesaemia. Our results show a two-fold increase in the prevalence of hypophosphataemia (plasma phosphate concentration < or = 0.80 mmol/l) in patients with hypomagnesaemia (plasma magnesium level < or = 0.70 mmol/l) compared with patients without this condition, and a six-fold increase in hypokalaemia (plasma potassium < or = 3.5 mmol/l). A triology consisting of hypomagnesaemia, hypophosphataemia and hypokalaemia is also described, which was found in 8% of patients with hypomagnesaemia and 17% of patients with severe hypomagnesaemia (plasma magnesium < or = 0.50 mmol/l). Patients most susceptible to this phenomenon include those in intensive therapy, post-operative patients, those with sepsis being treated with aminoglycosides, and oncology patients receiving chemotherapy.
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PMID:Hypophosphataemia and hypokalaemia in patients with hypomagnesaemia. 784 32

The capsular polysaccharide complex (CPC) of Bacteroides fragilis exhibits unusual biologic properties. This polysaccharide complex promotes the formation of abscesses and prevents abscess induction in a rat model of intra-abdominal sepsis. Each of these biologic properties is mediated by a T cell-dependent immune mechanism. The CPC consists of two distinct polysaccharides, PS A and PS B, each with repeating units that have positively charged amino groups and negatively charged carboxyl or phosphate groups. Analysis of these polysaccharides as well as other charged carbohydrates before and after chemical modification revealed that these oppositely charged groups are required for promotion of intra-abdominal abscesses as well as for protection against abscess induction. These studies provide a structural rationale for the distinct properties associated with the B. fragilis CPC, and delineate one mechanism by which this host response occurs.
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PMID:Bacterial structure and functional relation to abscess formation. 786 58

This study was performed to evaluate the effect of lactose induced diarrhea on the key enzymes of glutamine metabolism in skeletal muscle and small intestine, in rats. As compared to weight paired controls, animals with diarrhea presented higher muscle glutamine synthetase activity associated with reduced skeletal muscle glutamine concentration with a fall in arterial glutamine and an increased intestinal glutaminase activity. These alterations are similar to those reported by others in conditions in which accelerated muscle proteolysis is likely to occur such as in sepsis and after surgery. Besides the data suggestive of an overall alterations in glutamine metabolism, an important finding of this study was the increase in specific activity of intestinal phosphate dependent glutaminase in rats with diarrhea. This enzyme has been shown not to respond to many conditions such as acidosis, alkalosis or increased glutamine ingestion through drinking water or diet.
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PMID:Effect of lactose induced diarrhea on intestinal glutaminase and muscle glutamine synthetase activities in rats. 790 81

Gut fuel utilisation has several unique features. Arterial and luminal fuels provide nutrition for the enterocyte, the former being of more importance. This factor, and the heterogeneity of cell types within the gut makes it difficult to define its fuel utilisation. Metabolic control logic suggests that modulation of the maximal activity of any pathway resides in those enzymes that operate in vivo at rates far below their maximal capacity and that catalyse non-equilibrium reactions. On this basis, although enterocyte hexokinase activity is much higher than in other 'glycolytic' cells (for example, brain), potentially high rates of glucose utilisation are modulated by substrate cycling of glucose 6-phosphate back to glucose through glucose 6-phosphatase. Glutamine metabolism proceeds by glutaminase to produce glutamate, which may then be transaminated (aspartate-aminotransferase and alanine-amino transferase) to produce alpha-ketoglutarate, alanine, and aspartate. The end products of glutamine metabolism by incubated gut preparations in vitro (mainly alanine), suggests that enterocytes, not immune cells, are responsible for most gut glutamine metabolism. High flux rates of glucose and glutamine metabolism in the enterocyte may result from the need for de novo synthesis of purines and pyrimidines and ribose sugars for nucleic acid synthesis. Sepsis reduces rates of glucose and glutamine metabolism, perhaps to preserve the increased consumption of these fuels by activated lymphocytes and macrophages in the gut wall.
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PMID:Quantitative aspects of glucose and glutamine metabolism by intestinal cells. 812 83


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