Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 71 patients with fever and bacteremia without complications, a prospective study of acute-phase reactants is done. Raises in haptoglobin, ceruloplasmin, alpha-1-antitrypsin, protein C, beta-2-microglobulin, IgA and ferritin serum levels, together with leucocytosis and GSR, were very significant when diagnosis was done. Fibronectin, sideremia and transferrin were lowered. After 3 and 6 days of treatment haptoglobins, alpha-1-antitrypsin, protein C, ferritin, leucocytosis and GSR are lowered, while immunoglobulins, sideremia, transferrin and fibronectin raised, the latter until normalization. Fibronectin as well as changes in iron metabolism were very reliable parameters of inflammation and favorable evolution.
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PMID:[Acute-phase reactants in sepsis]. 148 35

Fibronectin is an adhesive glycoprotein that may influence the permeability of the vascular barrier. We compared the plasma disappearance of purified human fibronectin (hFn) and its incorporation into lung tissue in control nonbacteremic and bacteremic sheep after surgery to determine the influence of postoperative bacteremia on the plasma clearance and lung deposition of hFn. Lymph fistulas were surgically prepared 48 h before either saline or bacterial challenge to allow for collection of timed samples of plasma, lung lymph, and peripheral lymph. On the day of the study, the sheep were anesthetized and given either 5 X 10(8) Pseudomonas aeruginosa in saline or saline alone. In parallel, they were infused intravenously with 100 mg of hFn, and the hFn concentration in plasma, lymph, and tissue extracts was subsequently determined by enzyme-linked immunosorbent assay over an 8-h experimental interval. Localization of endogenous sheep fibronectin (sFn) and the injected hFn in serial lung tissue samples was determined by dual-label immunofluorescence. In nonbacteremic control sheep, plasma hFn levels declined with an initial rapid slope (t1/2 = 0.53 +/- 0.19 min), followed by a second, gradual slope (t1/2 = 21.7 +/- 2.5 h), whereas the concentration of hFn in lung lymph and peripheral lymph rose exponentially with time. In bacteremic sheep, the early plasma disappearance of hFn was similar, but the second phase of plasma clearance was faster (t1/2 = 7.4 +/- 0.3 h). Lung tissue from control and bacteremic sheep contained the same level of extractable hFn. However, tissue extraction followed by immunofluorescence microscopy indicated that lung tissue from bacteremic sheep contained more nonextractable hFn than lung tissue from nonbacteremic sheep. Thus postoperative bacteremia that elicits acute lung vascular injury will increase the plasma disappearance of hFn and its incorporation into the lung tissue.
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PMID:Kinetics of plasma fibronectin: increased lung tissue incorporation after postoperative bacteremia. 170 59

The propensity of Staphylococcus aureus to cause acute endovascular infections during transient bacteremia is poorly understood. To examine the events leading to the attachment of staphylococci to endothelium, adherence assays were developed to study the role of blood factors in the mediation of staphylococcal adherence to cultured human umbilical vein endothelium in vitro. Results indicate that the preferential attachment of S. aureus to endothelial cells is mediated by fibrinogen adsorbed from plasma onto the endothelial surface. The binding is apparently specific because it could be blocked by goat anti-human fibrinogen antibody in a dose-dependent fashion while nonimmune goat IgG, mouse MAb against AG-1 (a platelet antigen found on the endothelial cell surface), nonspecific mouse MAb and rabbit antibodies to human vitronectin and fibronectin were not inhibitory. Our data also indicate that fibrinogen is a necessary but not the only blood constituent in the mediation of binding of S. aureus to endothelium. This was supported by the finding that fibrinogen alone, at a concentration equivalent to that in plasma, did not potentiate staphylococcal adherence as much as plasma while afibrinogenemic plasma reconstituted with fibrinogen did. Because fibrinogen is known to bind to endothelial cells, our data is consistent with the hypothesis that fibrinogen and additional plasma factor(s), possibly activated during inflammation, promote staphylococcal adherence to endothelium. In addition, the role of the fibrinogen binding receptor of S. aureus as an adherence factor to native endothelium is also suggested.
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PMID:Fibrinogen acts as a bridging molecule in the adherence of Staphylococcus aureus to cultured human endothelial cells. 171 Feb 35

We studied the plasma clearance and tissue incorporation of intravenously infused purified human plasma fibronectin into various tissues during a period of acute lung vascular injury induced by lethal postoperative bacteremia in sheep. Lung, liver, spleen, and heart tissue were examined for both endogenous sheep tissue fibronectin as well as the experimentally infused human fibronectin using dual-label immunofluorescence. Awake sheep (n = 4) received a postoperative iv infusion of 5 x 10(9) live Pseudomonas over a 60-min infusion interval. Bacterial challenge was started 2 hr after starting the iv fibronectin infusion of purified human plasma fibronectin (100 mg iv bolus; 4 hr iv at 100 mg/hr). Human fibronectin displayed a biphasic rate of clearance from the plasma with entrance into lymph. Human fibronectin readily incorporated in all tissues studied, including the lung which was the focus of vascular injury. Analysis of tissue sections by dual-label immunofluorescence indicated that the exogenous human fibronectin colocalized with the endogenous sheep fibronectin. Thus, the plasma fibronectin concentration may influence the lung vascular barrier due to its incorporation into the tissue pool of fibronectin. Moreover, the plasma may serve as a reservoir for soluble fibronectin which can enter and colocalize with the insoluble tissue pool of fibronectin in various tissues.
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PMID:Incorporation of circulating fibronectin into various tissues during sepsis: colocalization with endogenous tissue fibronectin. 174 11

Bacteremia from gram-negative rods is a great cause of concern for hospital physicians today. Shock-complicating gram-negative sepsis has a mortality rate of 60% and above, despite early diagnosis and treatment. Intensive research efforts have shown new pathophysiological mechanisms and mediators involved in septic shock, with changes in recommended treatment protocols. In this report, the authors review the use of corticosteroids, fibronectin, naloxone hydrochloride, and immunotherapy, with emphasis on theoretical considerations and relevant clinical experience. Although these treatment methods may have been promising initially, data from large double-blind human trials are either lacking or unencouraging. While continued research and modern therapeutic approaches should improve future survival rates from septic shock, use of the therapies reviewed should be considered experimental at this time.
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PMID:Modern approaches to the therapy of septic shock. 240 67

Fibronectin is found in plasma as well as in association with connective tissue and cell surfaces. Depletion of plasma fibronectin is often observed in septic trauma and burned patients, while experimental rats often manifest hyperfibronectinemia with sepsis. Since Factor XIII may influence the rate of clearance and deposition of plasma fibronectin into tissues, we evaluated the temporal changes in plasma fibronectin and plasma Factor XIII following bacteremia and RE blockade in rats in an attempt to understand the mechanism leading to elevation of fibronectin levels in bacteremic rats, which is distinct from that observed with RE blockade. Clearance of exogenously administered fibronectin after bacteremia was also determined. Rats received either saline, Pseudomonas aeruginosa (1 X 10(9) organisms), gelatinized RE test lipid emulsion (50 mg/100 gm B.W.), or emulsion followed by Pseudomonas. Plasma fibronectin and Factor XIII were determined at 0, 2, 24, and 48 hours post-blockade or bacteremia. At 24 and 48 hr following bacteremia alone or bacteremia after RE blockade, there was a significant elevation (p less than 0.05) of plasma fibronectin and a concomitant decrease (p less than 0.05) of plasma factor XIII activity. Extractable tissue fibronectin from liver and spleen was also increased at 24 and 48 hours following R.E. blockade plus bacteremia. In addition, the plasma clearance of human fibronectin was significantly prolonged (p less than 0.05) following bacterial challenge. Infusion of activated Factor XIII (20 units/rat) during a period of hyperfibronectinemia (908.0 +/- 55.1 micrograms/ml) resulted in a significant (p less than 0.05) decrease in plasma fibronectin (548.5 +/- 49.9 micrograms/ml) within 30 min. Thus Factor XIII deficiency in rats with bacteremia may contribute to the elevation in plasma fibronectin by altering kinetics associated with the clearance of fibronectin from the blood.
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PMID:Factor XIII as a modulator of plasma fibronectin alterations during experimental bacteremia. 287 87

Bacterial adherence to polymer surfaces is a required early step in intravenous (iv) device infection. We collected eight strains of Staphylococcus aureus and 19 of coagulase-negative staphylococci from patients with proven iv device bacteremia and studied the role of plasma or connective-tissue proteins in promoting bacterial adherence to polymethylmethacrylate (PMMA) coverslips. Although only a negligible percentage of organisms adhered to albumin-coated PMMA, surface-bound fibronectin significantly promoted adherence of all isolates. Fibrinogen markedly promoted adherence of all S. aureus strains but of only four coagulase-negative strains. Thus, coagulase-negative staphylococci revealed a marked heterogeneity in adherence to fibrinogen-coated surfaces, a result suggesting the existence of heretofore unknown receptors for fibrinogen. Laminin promoted adherence of staphylococci to a much lower extent. Although strain specific, adherence of clinical staphylococcal isolates to foreign surfaces is significantly increased by fibronectin, fibrinogen, and laminin, an observation suggesting the possible contribution of these proteins to the pathogenesis of iv device infection.
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PMID:Fibronectin, fibrinogen, and laminin act as mediators of adherence of clinical staphylococcal isolates to foreign material. 317 Dec 24

An increase in pulmonary transvascular protein clearance is seen in sheep following postoperative bacteremia. We evaluated whether this increased protein clearance is specific for the lung by comparing in sheep the effect of postoperative bacteremia on both pulmonary and prefemoral lymph protein clearance. Fibronectin, implicated as a factor influencing vascular permeability, was also measured. After intravenous infusion of a sublethal dose of 5 x 10(8) live Pseudomonas aeruginosa (n = 10), pulmonary lymph flow (QL) increased 146% (P less than 0.01), and the lung lymph-to-plasma (L/P) total protein concentration ratio increased 21% (P less than 0.05). This resulted in a 208% elevation (P less than 0.01) in lung protein clearance (LPC = QL x L/P). In contrast, peripheral lymph flow and peripheral protein clearance were not altered. After intravenous infusion of a lethal dose of 5 x 10(9) live Pseudomonas (n = 7), QL rose 243-348% (P less than 0.025), whereas the lung L/P remained at base line, resulting in a 240-358% increase in LPC (P less than 0.025). Again, peripheral lymph flow and protein clearance did not increase. Plasma fibronectin declined slightly after low-dose bacterial challenge but decreased (P less than 0.001) 40% by 4-5 h after high-dose bacterial challenge. After both low- and high-dose bacterial challenge, fibronectin in pulmonary lymph increased (P less than 0.05) relative to total protein. In contrast, no change in peripheral lymph fibronectin was seen. Thus, while postoperative bacteremia increased lung protein clearance, it did not increase peripheral protein clearance, suggesting specificity with regard to the microvascular response to bacteremia.
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PMID:Pulmonary and peripheral lymph protein clearance during bacteremia after surgery. 320 5

Plasma fibronectin levels and complete blood cell counts were assessed prospectively among 100 infants less than 3 months of age with the provisional diagnosis of "possible sepsis". Seven of the ten infants with culture-proved bacteremia, meningitis, or urinary tract infection had low plasma fibronectin levels as did 12 (13%) of 90 infants with superficial or no documented bacterial infection. The positive predictive value of a low plasma fibronectin level in conjunction with leukocytosis and elevated band ratio for discriminating serious bacterial infection was 71%. Normal white blood cell counts or fibronectin level alone or in combination predicted the absence of serious bacterial infection with an accuracy of at least 94%. Plasma fibronectin determination provides a useful adjunct to the complete blood cell count for the rapid evaluation of extent of illness in young infants with possible sepsis.
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PMID:Role of fibronectin in diagnosing bacterial infection in infancy. 339 79

Collagen binding was examined in 90 strains of Staphylococcus aureus derived from patient samples. Slightly under one-half (39 of 90) of the S. aureus strains bound collagen. Collagen binding in S. aureus did not correlate with either immunoglobulin G or fibronectin binding by these organisms. Chi-square analysis of isolates obtained from patients with complicated bacteremia (bacteremia associated with deep tissue infection) compared with isolates from patients with uncomplicated bacteremia (bacteremia without other infection) showed that the former strains were significantly more likely to have collagen-binding ability. Subcloning of primary isolates from patients with bacteremia showed that all clones from individual patients were either all positive for collagen binding or all negative, suggesting a common clonal origin for this characteristic. The ability to bind collagen could not be induced in strains lacking collagen affinity by repeated subculture in media supplemented with collagen.
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PMID:Collagen binding in clinical isolates of Staphylococcus aureus. 342 18


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