fibrin and Pseudomonas-Infections

fibrin has been researched along with Pseudomonas-Infections* in 10 studies

Trials

1 trial(s) available for fibrin and Pseudomonas-Infections

ArticleYear
Phosphatidylserine externalization and procoagulant activation of erythrocytes induced by Pseudomonas aeruginosa virulence factor pyocyanin.
    Journal of cellular and molecular medicine, 2016, Volume: 20, Issue:4

    The opportunistic pathogen Pseudomonas aeruginosa causes a wide range of infections in multiple hosts by releasing an arsenal of virulence factors such as pyocyanin. Despite numerous reports on the pleiotropic cellular targets of pyocyanin toxicity in vivo, its impact on erythrocytes remains elusive. Erythrocytes undergo an apoptosis-like cell death called eryptosis which is characterized by cell shrinkage and phosphatidylserine (PS) externalization; this process confers a procoagulant phenotype on erythrocytes as well as fosters their phagocytosis and subsequent clearance from the circulation. Herein, we demonstrate that P. aeruginosa pyocyanin-elicited PS exposure and cell shrinkage in erythrocyte while preserving the membrane integrity. Mechanistically, exposure of erythrocytes to pyocyanin showed increased cytosolic Ca(2+) activity as well as Ca(2+) -dependent proteolytic processing of μ-calpain. Pyocyanin further up-regulated erythrocyte ceramide abundance and triggered the production of reactive oxygen species. Pyocyanin-induced increased PS externalization in erythrocytes translated into enhanced prothrombin activation and fibrin generation in plasma. As judged by carboxyfluorescein succinimidyl-ester labelling, pyocyanin-treated erythrocytes were cleared faster from the murine circulation as compared to untreated erythrocytes. Furthermore, erythrocytes incubated in plasma from patients with P. aeruginosa sepsis showed increased PS exposure as compared to erythrocytes incubated in plasma from healthy donors. In conclusion, the present study discloses the eryptosis-inducing effect of the virulence factor pyocyanin, thereby shedding light on a potentially important mechanism in the systemic complications of P. aeruginosa infection.

    Topics: Adult; Aged; Aged, 80 and over; Blood Coagulation; Calcium; Calpain; Cations, Divalent; Ceramides; Eryptosis; Erythrocytes; Female; Fibrin; Humans; Ion Transport; Male; Middle Aged; Phosphatidylserines; Prothrombin; Pseudomonas aeruginosa; Pseudomonas Infections; Pyocyanine; Reactive Oxygen Species; Sepsis; Virulence Factors

2016

Other Studies

9 other study(ies) available for fibrin and Pseudomonas-Infections

ArticleYear
A PEGylated fibrin hydrogel-based antimicrobial wound dressing controls infection without impeding wound healing.
    International wound journal, 2017, Volume: 14, Issue:6

    Combat injuries are associated with a high incidence of infection, and there is a continuing need for improved approaches to control infection and promote wound healing. Due to the possible local and systemic adverse effects of standard 1% cream formulation (Silvadene), we had previously developed a polyethylene glycol (PEGylated) fibrin hydrogel (FPEG)-based wound dressing for the controlled delivery of silver sulfadiazine (SSD) entrapped in chitosan microspheres (CSM). In this study, we have evaluated the antimicrobial and wound healing efficacy of SSD-CSM-FPEG using a full-thickness porcine wound infected with Pseudomonas aeruginosa. Infected wounds treated with a one-time application of the SSD-CSM-FPEG wound dressing demonstrated significantly reduced bacterial bioburden over time (99·99% of reduction by day 11; P < 0·05) compared with all the other treatment groups. The epithelial thickness and granulation of the wound bed was significantly better on day 7 (150·9 ± 13·12 µm), when compared with other treatment groups. Overall, our findings demonstrate that the SSD-CSM-FPEG wound dressing effectively controls P. aeruginosa infection and promotes wound healing by providing a favourable environment that induces neovascularisation. Collectively, sustained release of SSD using fibrin hydrogel exhibited enhanced benefits when compared with the currently available SSD treatment, and this may have significant implications in the bacterial reduction of infected wounds in military and civilian populations.

    Topics: Animals; Anti-Infective Agents, Local; Bandages, Hydrocolloid; Chitosan; Disease Models, Animal; Fibrin; Microspheres; Pseudomonas Infections; Silver Sulfadiazine; Swine; Wound Healing; Wounds and Injuries

2017
Pseudomonas aeruginosa toxin ExoU induces a PAF-dependent impairment of alveolar fibrin turnover secondary to enhanced activation of coagulation and increased expression of plasminogen activator inhibitor-1 in the course of mice pneumosepsis.
    Respiratory research, 2011, Aug-05, Volume: 12

    ExoU, a Pseudomonas aeruginosa cytotoxin with phospholipase A2 activity, was shown to induce vascular hyperpermeability and thrombus formation in a murine model of pneumosepsis. In this study, we investigated the toxin ability to induce alterations in pulmonary fibrinolysis and the contribution of the platelet activating factor (PAF) in the ExoU-induced overexpression of plasminogen activator inhibitor-1 (PAI-1).. Mice were intratracheally instilled with the ExoU producing PA103 P. aeruginosa or its mutant with deletion of the exoU gene. After 24 h, animal bronchoalveolar lavage fluids (BALF) were analyzed and lung sections were submitted to fibrin and PAI-1 immunohistochemical localization. Supernatants from A549 airway epithelial cells and THP-1 macrophage cultures infected with both bacterial strains were also analyzed at 24 h post-infection.. In PA103-infected mice, but not in control animals or in mice infected with the bacterial mutant, extensive fibrin deposition was detected in lung parenchyma and microvasculature whereas mice BALF exhibited elevated tissue factor-dependent procoagulant activity and PAI-1 concentration. ExoU-triggered PAI-1 overexpression was confirmed by immunohistochemistry. In in vitro assays, PA103-infected A549 cells exhibited overexpression of PAI-1 mRNA. Increased concentration of PAI-1 protein was detected in both A549 and THP-1 culture supernatants. Mice treatment with a PAF antagonist prior to PA103 infection reduced significantly PAI-1 concentrations in mice BALF. Similarly, A549 cell treatment with an antibody against PAF receptor significantly reduced PAI-1 mRNA expression and PAI-1 concentrations in cell supernatants, respectively.. ExoU was shown to induce disturbed fibrin turnover, secondary to enhanced procoagulant and antifibrinolytic activity during P. aeruginosa pneumosepsis, by a PAF-dependent mechanism. Besides its possible pathophysiological relevance, in vitro detection of exoU gene in bacterial clinical isolates warrants investigation as a predictor of outcome of patients with P. aeruginosa pneumonia/sepsis and as a marker to guide treatment strategies.

    Topics: Animals; Bacterial Proteins; Blood Coagulation; Bronchoalveolar Lavage Fluid; Cell Line, Tumor; Disease Models, Animal; Epithelial Cells; Female; Fibrin; Humans; Immunohistochemistry; Macrophages; Mice; Mutation; Plasminogen Activator Inhibitor 1; Platelet Activating Factor; Pneumonia, Bacterial; Pseudomonas aeruginosa; Pseudomonas Infections; Pulmonary Alveoli; Respiratory Mucosa; RNA, Messenger; Sepsis; Time Factors; Up-Regulation

2011
Binding of plasminogen to Pseudomonas aeruginosa results in formation of surface-associated plasmin and enhanced bacterial invasiveness.
    Microbial pathogenesis, 2004, Volume: 36, Issue:2

    The interaction of Pseudomonas aeruginosa with plasminogen (Plg) is herein reported. Plg bound similarly to laboratory and clinical P. aeruginosa isolates from blood of septicemic patients and stools of asymptomatic carriers. No difference in Plg capture was detected between the piliated PAK strain and its isogenic nonpiliated mutant. Western immunoblotting results suggested that low molecular weight nonpilus adhesins from the bacterial outer membranes accounted for the Plg capture. Bacteria-bound Plg was converted to bioactive plasmin in the presence of exogenous urokinase-type Plg activator. The presence of surface-bound plasmin enhanced significantly the P. aeruginosa capability to invade fibrin gels and a reconstituted basement membrane matrix. These findings support the concept that Plg capture by P. aeruginosa may represent a mechanism which offers advantages to bacterial invasiveness through tissue barriers.

    Topics: Adhesins, Bacterial; Bacterial Outer Membrane Proteins; Basement Membrane; Blood; Carrier State; Feces; Fibrin; Fibrinolysin; Fibrinolysis; Fimbriae, Bacterial; Humans; Movement; Plasminogen; Plasminogen Activators; Protein Binding; Pseudomonas aeruginosa; Pseudomonas Infections; Urokinase-Type Plasminogen Activator; Virulence

2004
Massive alveolar thrombin activation in Pseudomonas aeruginosa-induced acute lung injury.
    Shock (Augusta, Ga.), 2004, Volume: 21, Issue:5

    In acute lung injury (ALI), a coagulation/fibrinolysis imbalance leads to fibrin deposition, persistence of which contributes to fibrotic evolution. Our study evaluated the effects of early inhibition of coagulation in Pseudomonas aeruginosa (Pa)-induced ALI through the use of recombinant human antithrombin (rhAT). The study was conducted in vivo on a murine model of Pa-induced ALI. Intravenous rhAT was administered simultaneously with intratracheal Pa. Four experimental groups were compared: CTR, intratracheal saline (0.5 mL/kg)/intravenous saline (1 mL); PNP, intratracheal Pa (0.5 mL/kg of 2 x 10(9) cfu)/intravenous saline; AT, intratracheal saline/intravenous rhAT (500 IU/kg); ATPNP, intratracheal Pa/intravenous rhAT. Epithelial and endothelial permeabilities were evaluated with radiolabeled albumin flux across the alveolar barrier (125I- and 131I-labeled albumin). Thrombin-antithrombin (TAT) complexes levels were used as markers of coagulation activation in blood samples and in BAL fluid. Epithelial and endothelial protein permeability were increased in Pa-induced ALI versus control. Intravenous rhAT administration led to further permeability disorders. Administration of rhAT in Pa ALI led to a rise in TAT complexes in ATPNP blood serum and BAL fluids compared with the other groups. In Pa-induced ALI the administration intravenous rhAT leads to major histologic damage, alveolar capillary barrier injury, and permeability increase. Such effects of the inhibition of thrombin activation by rhAT lead to the hypothesis of a probable beneficial role of early coagulation activation in ALI as a factor limiting both the extent of injury and permeability disorders. Our study suggests that inhibition of this initial procoagulative imbalance is potentially dangerous.

    Topics: Animals; Antithrombins; Blood Coagulation; Blood Pressure; Bronchoalveolar Lavage Fluid; Female; Fibrin; Fibrinolysis; Humans; Lung; Lung Injury; Oxygen; Pseudomonas aeruginosa; Pseudomonas Infections; Pulmonary Alveoli; Rats; Rats, Sprague-Dawley; Respiratory Distress Syndrome; Thrombin; Time Factors

2004
Differential distributions in tissues and efficacies of aztreonam and ceftazidime and in vivo bacterial morphological changes following treatment.
    Antimicrobial agents and chemotherapy, 1997, Volume: 41, Issue:2

    The differential tissue distributions of aztreonam and ceftazidime within fibrin clots infected with Pseudomonas aeruginosa, Enterobacter cloacae, and Serratia marcescens, their efficacies, and the in vivo bacterial morphological changes induced by these drugs were evaluated. Rabbits were given intravenously a single dose of 100 mg of either agents/kg of body weight. In the cores of the clots, the peak levels of both drugs were much lower than those observed in the peripheries and in serum. Aztreonam's half-lives within the peripheries and in the cores of the fibrin clots were up to six times higher than observed in serum, while ceftazidime's half-lives in clots were twice that observed in serum. This resulted in a much greater penetration ratio for aztreonam than for ceftazidime. Both drugs controlled the growth of P. aeruginosa in vivo, but E. cloacae and S. marcescens responded better to ceftazidime. Morphological changes were more abundant in the peripheries than in the cores of the clots. In the control group, P. aeruginosa's morphology in the cores was different than that in the peripheries of the clots. Against P. aeruginosa, aztreonam did induce morphological changes in the cores while ceftazidime did not. Electron microscopic studies revealed that morphological changes associated with aztreonam seemed different than those of ceftazidime. Along with elongation of bacteria, more bow tie and herniated bacteria were observed with aztreonam. Though both agents selectively affect PBP 3, as manifested by elongated bacteria, they induce in the peripheries of the clots thickening, breaks, and detachment in bacterial cell walls, alterations which are generally associated with antibiotics affecting PBP 1a and 1b.

    Topics: Animals; Aztreonam; Ceftazidime; Cephalosporins; Enterobacter cloacae; Enterobacteriaceae Infections; Female; Fibrin; Microbial Sensitivity Tests; Monobactams; Pseudomonas aeruginosa; Pseudomonas Infections; Rabbits; Serratia Infections; Serratia marcescens

1997
Fibrin-enmeshed tobramycin liposomes: single application topical therapy of Pseudomonas keratitis.
    Cornea, 1992, Volume: 11, Issue:5

    Treatment of bacterial keratitis requires frequent application of topical antibiotics. We studied the efficacy of a single topical administration of tobramycin incorporated in large multivesicular liposomes and enmeshed in a fibrin sealant on rabbit corneas infected with Pseudomonas aeruginosa. One cornea each of 25 New Zealand albino rabbits was infected with P. aeruginosa. Twenty-four hours later, the animals were randomly divided into five groups of five. Group A received single hourly drops (50 microliters) of fortified tobramycin (14.5 mg/ml, total of 17.4 mg). Group B received a single topical application of 3.5 mg tobramycin, in 0.1 ml multivesicular liposomes, enmeshed in a fibrin sealant with an overlaying bandage contact lens. Group C was treated in the same manner as group B without the addition of fibrin sealant. Groups D and E served as nondrug-treated controls, with group D receiving topical fibrin-enmeshed liposomes devoid of tobramycin and group E receiving hourly topical balanced salt solution (BSS) drops. All animals were killed 24 h after initiation of therapy. Significantly fewer colonies of Pseudomonas were present in corneas of all three treated groups, as compared with the two nondrug-treated control groups (p less than 0.02). There were significantly fewer colonies of Pseudomonas in groups A and B as compared with group C (p less than 0.02). No significant difference was noted between a single administration of topical fibrinen-meshed tobramycin-encapsulated liposomes (group B) and 24 doses of hourly fortified topical tobramycin (group A, p greater than 0.05). Tobramycin-encapsulated megaliposomes may serve as a useful adjunct in treatment of Pseudomonas keratitis.

    Topics: Administration, Topical; Animals; Colony Count, Microbial; Cornea; Corneal Ulcer; Disease Models, Animal; Drug Carriers; Eye Infections, Bacterial; Fibrin; Liposomes; Pseudomonas aeruginosa; Pseudomonas Infections; Rabbits; Random Allocation; Tobramycin

1992
Intracameral tissue plasminogen activator for treatment of excessive fibrin response after penetrating keratoplasty.
    American journal of ophthalmology, 1990, Apr-15, Volume: 109, Issue:4

    Topics: Aged; Anterior Chamber; Corneal Ulcer; Eye Infections, Bacterial; Fibrin; Fibrinolysis; Humans; Injections; Keratoplasty, Penetrating; Male; Pseudomonas Infections; Tissue Plasminogen Activator

1990
The early diagnosis of gram negative septicemia in the pediatric surgical patient.
    Annals of surgery, 1975, Volume: 182, Issue:3

    Ninety-three postoperative patients 1 day to 13 years of age had blood cultures, limulus lysate assay, determination of fibrin degradation products, white blood cell and platelet counts. Seven groups were studied. The limulus lysate assay was often positive (64%) in the presence of gram negative septicemia but there were false positives and negatives. The tests for fibrin degradation products were inconsistent. The white blood cell count was low in babies with gram negative septicemia. One hundred per cent of the infants with gram negative septicemia had a platelet count below 150,000; 71% below 100,000 (average 67,000 septic babies, 257,000 non-septic babies). The drop in platelet count with gram negative septicemia was abrupt---as much as 222,000 in 24 hours. Platelets increased when therapy was effective. Two children with gram negative septicemia had platelet counts of 50,000 and 20,000. The platelet count for patients with gram positive septicemia was 299,000, and above 150,000 in all children with ruptured and non-ruptured appendicitis and major surgery without gram negative septicemia. It was concluded that serial measurements of platelet count in the postoperative infant and child was a rapid and reliable method for early detection of gram negative septicemia and changes in platelet count in response to treatment was an indicator of the effectiveness of therapy.

    Topics: Abdominal Muscles; Adolescent; Appendicitis; Bacteria; Bacterial Infections; Blood Cell Count; Blood Platelets; Child; Child, Preschool; Enterocolitis, Pseudomembranous; Escherichia coli Infections; Fibrin; Gangrene; Humans; Infant; Infant, Newborn; Intestinal Obstruction; Klebsiella Infections; Leukocyte Count; Liver Neoplasms; Platelet Aggregation; Postoperative Complications; Pseudomonas Infections; Sepsis; Time Factors

1975
Pseudomonas corneal ulceration: an electron microscopic study.
    Annals of ophthalmology, 1973, Volume: 5, Issue:11

    Topics: Administration, Topical; Adult; Basement Membrane; Collagen; Cornea; Corneal Ulcer; Edema; Epithelium; Fibrin; Gentamicins; Humans; Inclusion Bodies; Leukocytes; Macrophages; Male; Microscopy, Electron; Pseudomonas aeruginosa; Pseudomonas Infections

1973
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