scholarly journals Alterations of Plasmin Activity, Plasminogen Levels and Activity of Anti-Plasmins During Endotoxin Shock in Dogs

1977 ◽  
Author(s):  
A. O. Aasen ◽  
M. J. Gallimore ◽  
K. Ohlsson ◽  
E. Amundsen
Keyword(s):  
Intravenous Infusion ◽  
Lethal Dose ◽  
Endotoxin Shock ◽  
Time Dependent ◽  
Plasmin Activity ◽  
Endotoxin Infusion ◽  
E Coli ◽  
Research Division ◽  
Late Stages

Endotoxin shock was induced in dogs by intravenous infusion of a lethal dose of E. coli endotoxin over a period of 3 hours. Typical changes of cardiovascular parameters were found and evidence of an intravascular clotting process was observed. Spontaneous plasmin activity and “immediate” and “time dependent” antiplasmin activities were determined by means of assays utilizing the chromogenic tripeptide derivative S-2251(Kabi Peptide Research Division, Mölndal, Sweden). Levels of plasminogen, α2-macrolobulin (α2-M) , and ai-antitrypsin(α1-AT) were determined immunochemically. During shock, gradually decreasing values of “immediate” antiplasmin and α2M were observed. During the late stages of shock “immediate” antiplasmin was found to be reduced by up to 89 per cent and α2M up to 50 per cent of pre endotoxin infusion values. A less marked lowering of “time dependent” antiplasmin and α1-AT also occurred during shock. These changes of plasma antiplasmins were accompanied by decreasing values of plasminogen and evidence of plasmin activity. These findings indicate that plasminogen is converted to plasmin during endotoxin shock and emphasize the role of antiplasmins in the pathophysiology of endotoxin shock.

scholarly journals Bacterial Dose-Dependent Role of G Protein-Coupled Receptor Kinase 5 in Escherichia coli-Induced Pneumonia

2016 ◽  
Vol 84 (5) ◽  
pp. 1633-1641 ◽  
Author(s):  
Nandakumar Packiriswamy ◽  
Michael Steury ◽  
Ian C. McCabe ◽  
Scott D. Fitzgerald ◽  
Narayanan Parameswaran
Keyword(s):  
Escherichia Coli ◽  
G Protein ◽  
Lethal Dose ◽  
Neutrophil Recruitment ◽  
Sublethal Dose ◽  
Receptor Kinase ◽  
Content Type ◽  
E Coli ◽  
G Protein Coupled

G protein-coupled receptor kinase 5 (GRK5) is a serine/threonine kinase previously shown to mediate polymicrobial sepsis-induced inflammation. The goal of the present study was to examine the role of GRK5 in monomicrobial pulmonary infection by using an intratrachealEscherichia coliinfection model of pneumonia. We used sublethal and lethal doses ofE. colito examine the mechanistic differences between low-grade and high-grade inflammation induced byE. coliinfection. With a sublethal dose ofE. coli, GRK5 knockout (KO) mice exhibited higher plasma CXCL1/KC levels and enhanced lung neutrophil recruitment early after infection, and lower bacterial loads, than wild-type (WT) mice. The inflammatory response was also diminished, and resolution of inflammation advanced, in the lungs of GRK5 KO mice. In contrast to the reduced bacterial loads in GRK5 KO mice following a sublethal dose, at a lethal dose ofE. coli, the bacterial burdens remained high in GRK5 KO mice relative to those in WT mice. This occurred in spite of enhanced plasma CXCL1 levels as well as neutrophil recruitment in the KO mice. But the recruited neutrophils (following high-dose infection) exhibited decreased CD11b expression and reduced reactive oxygen species production, suggesting decreased neutrophil activation or increased neutrophil exhaustion in the GRK5 KO mice. In agreement with the increased bacterial burden, KO mice showed poorer survival than WT mice followingE. coliinfection at a lethal dose. Overall, our data suggest that GRK5 negatively regulates CXCL1/KC levels during bacterial pneumonia but that the role of GRK5 in the clinical outcome in this model is dependent on the bacterial dose.

scholarly journals Changes in Levels of Plasma Pre-Kallikrein, Kallikrein and Kallikrein Inhibitors During Endotoxin Shock in Dogs

1977 ◽  
Author(s):  
M. J. Gallimore ◽  
A. O. Aasen ◽  
E. Amundsen
Keyword(s):  
Late Phase ◽  
Endotoxin Shock ◽  
Time Dependent ◽  
Plasma Kallikrein ◽  
Kinin System ◽  
E Coli ◽  
Dependent Inhibition ◽  
Kallikrein Kinin System ◽  
Time Dependent Inhibition ◽  
Kallikrein Inhibitors

Plasma protease activity is known to be increased during endotoxin shock and recent studies have indicated that the plasma kallikrein-kinin system becomes activated by circulating endotoxin. Plasma levels of pre-kallikrein kallikrein and kallikrein inhibitors were therefore determined in samples from dogs infused with E. coli endotoxin, using assays with a chromogenic substrate for plasma kallikrein(Chromozyme -PK, Pentapharm, Basle, Switzerland). “Fast-reacting” and “time-dependent” inhibitors of kallikrein were studied using purified human plasma kallikrein. Considerably reduced levels of plasma pre-kallikreiri and increased levels of kallikrein were detected in the late phase of shock and significant reductions in “fast-reacting” and “time-dependent” inhibition of kallikrein was observed. These results show that during endotoxin shock plasma pre-kallikrein becomes activated to kallikrein and indicate that kallikrein inhibitors play an important mediatory role in the pathophysiology of endotoxin shock.

Protection by histamine and metabolites in anaphylaxis, scalds, and endotoxin shock

1962 ◽  
Vol 202 (1) ◽  
pp. 111-113 ◽  
Author(s):  
Charles L. Fox ◽  
Sigmund E. Lasker
Keyword(s):  
Horse Serum ◽  
Lethal Factor ◽  
Lethal Dose ◽  
Active Role ◽  
Endotoxin Shock ◽  
E Coli ◽  
Thermal Burns ◽  
Scald Injury ◽  
Toxic Factors

The release of toxic factors has been implicated in the mechanism of shock from various forms of trauma. If histamine (H) released after anaphylaxis, endotoxin shock, or thermal burns is a lethal factor in mice, priming with (H) before injury would presumably enhance mortality. Mice were pretreated with (H) or certain metabolites prior to inducing shock via horse serum anaphylaxis, scald injury, or lethal dose of E. coli endotoxin. Large doses of (H) did not enhance mortality; actually, mortality from these three forms of shock was lowered by pretreatment with (H) or imidazoleacetic acid, but not by other metabolites tested. The data, while unexplained, do not appear to support hypotheses assigning an active role to (H) release in these three forms of shock in mice.

scholarly journals A LABILE SERUM FACTOR IN EXPERIMENTAL ENDOTOXIN SHOCK: CROSS-TRANSFUSION STUDIES IN DOGS

1961 ◽  
Vol 114 (4) ◽  
pp. 501-508 ◽  
Author(s):  
Wesley W. Spink ◽  
James Vick
Keyword(s):  
Lethal Dose ◽  
Endotoxin Shock ◽  
Serum Factor ◽  
Initial Stage ◽  
Endotoxin Activity ◽  
Plasma Factor ◽  
Liberation Of Histamine ◽  
Control Adult

Peripheral vascular failure caused by endotoxin in the dog has an initial stage of vasoconstriction. Preliminary studies in vitro demonstrated that the constriction was due to the interaction of endotoxin with a heat-labile serum or plasma factor and platelets, resulting in the liberation of histamine. Further studies on the intact dog support and extend this concept. A standardized dose of Escherichia coli endotoxin produced fatal shock in control adult mongrel dogs within 28 hours. The characteristic pattern of changes included progressive hypotension, oliguria and anuria, hemoconcentration, and acidosis. Normal dogs were protected against endotoxin by transfusions of blood in which the essential serum factor was depleted in one of two ways. First, plasma separated from the blood of normal animals was heated at 56°C for 30 minutes, and the infused reconstituted whole blood protected normal dogs. Protection was not afforded by unheated reconstituted blood. Second, blood from immune dogs obtained within 24 hours after a second lethal dose of endotoxin protected recipient dogs. However, protection was not demonstrated with blood collected 72 hours after a second injection of endotoxin. The nature of the serum factor essential for endotoxin activity is not known. It is postulated that an enzyme or enzyme system is involved, and the possible role of complement is discussed.

Mechanism of histamine release in endotoxin shock

1961 ◽  
Vol 200 (5) ◽  
pp. 987-989 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Margaret M. Jordan ◽  
James A. Vick
Keyword(s):  
Histamine Release ◽  
Active Role ◽  
Endotoxin Shock ◽  
Hemodynamic Changes ◽  
Endotoxin Administration ◽  
E Coli ◽  
Anesthetized Dogs ◽  
Blood Histamine ◽  
Lethal Doses

Reports from this laboratory have dealt with hemodynamic changes after injection of endotoxin and the role of histamine in endotoxin shock. This study relates to the mechanism of histamine release. Anesthetized dogs were administered lethal doses of E. coli endotoxin. During the course of the subsequent hypotension, simultaneous increases of blood histamine, histamine-histidine ratio(H/Hd), and circulating hematocrit were observed. Results suggest that a conversion from histidine to histamine occurs at an accelerated rate following endotoxin administration. These findings give further evidence for the active role of histamine in endotoxin shock and support a hypothesis recently proposed by Schayer.

Glucose utilization and role of blood in endotoxin shock.

1977 ◽  
Vol 233 (2) ◽  
pp. E71
Author(s):  
L B Hinshaw ◽  
L T Archer ◽  
B K Beller ◽  
G L White ◽  
T M Schroeder ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Glucose Utilization ◽  
Lactic Acid Production ◽  
White Blood Cells ◽  
Endotoxin Shock ◽  
E Coli ◽  
Predicted Values

The present study was conducted to explore influences modifying glucose uptake in canine blood administered LD100 E. coli endotoxin. Particular emphasis was given to assay the role of the white blood cell (WBC) in glucose utilization. Significant increases in glucose uptake and lactic acid production, attributed to increased activity of the WBC, were observed 1-3 h after endotoxin was added to blood in vitro. Although a net increase in glucose utilization was noted, endotoxin simultaneously exerted adverse effects by depressing glucose uptake below predicted values (Q10 = 2.12 with LD100 endotoxin vs. 2.78 in saline controls) and increasing WBC mortality rate. Blood from dogs pretreated with sublethal doses of endotoxin in vivo utilized glucose at an accelerated rate when subjected to endotoxin in vitro. Excess glucose was consumed because of elevated numbers of white blood cells although additional glucose requirements after endotoxin were independent of temperature between the ranges of 34-41 degrees C. All animals pretreated with daily sublethal injections of endotoxin for 3 days survived superlethal doses of endotoxin.

scholarly journals The role of 5-hydroxytryptamine in the feline response to intravenous infusion of live E. coli

1983 ◽  
Vol 79 (3) ◽  
pp. 711-718 ◽  
Author(s):  
S. Arvidsson ◽  
A. Falk ◽  
E. Haglind ◽  
U. Haglund
Keyword(s):  
Intravenous Infusion ◽  
E Coli

scholarly journals Effect of Biochar on the Production of L-Histidine From Glucose Through Escherichia coli Metabolism

2021 ◽  
Vol 8 ◽  
Author(s):  
Yang E ◽  
Jun Meng ◽  
Heqing Cai ◽  
Caibin Li ◽  
Sainan Liu ◽  
...  
Keyword(s):  
Organic Compounds ◽  
Traditional Method ◽  
Organic Molecules ◽  
Lethal Dose ◽  
The Other ◽  
Related Gene ◽  
High Concentration ◽  
E Coli ◽  
Hormone Analogs

The organic compounds from biochar play a role of hormone analogs, stimulating the expression of metabolites by controlling related gene and protein. In this experiment, we reported the L-histidine biosysthesis was promoted by biochar treatment in E. coli unlike genetic engineering of the traditional method. The related results indicated the most optimal concentration was found to be 3%, and 7% is the lethal dose. E. coli was inhibited in the high-concentration treatment. On the other hand, docking technology was usually used as drug screening, basing on Lock-and-key model of protein in order to better understand mechanisms. So the organic compounds of biochar from GC-MS analysis that acted as ligands were connected to HisG protein controlling L-histidine biosysthesis in E. coli. The result showed that the three organic molecules interacted with HisG protein by hydrogen bond. So we considered that these three compounds play regulatory roles in L-histidine biosysthesis, and the hisG gene expression fully supports this conclusion.

scholarly journals Genetic Evidence that GTP Is Required for Transposition of IS903 and Tn552 in Escherichia coli

2005 ◽  
Vol 187 (13) ◽  
pp. 4598-4606 ◽  
Author(s):  
Abbie M. Coros ◽  
Erin Twiss ◽  
Norma P. Tavakoli ◽  
Keith M. Derbyshire
Keyword(s):  
Escherichia Coli ◽  
Developmental Stage ◽  
Biosynthetic Pathway ◽  
Spatial Location ◽  
Colony Growth ◽  
Host Factors ◽  
Mutant Library ◽  
E Coli ◽  
Late Stages

ABSTRACT Surprisingly little is known about the role of host factors in regulating transposition, despite the potentially deleterious rearrangements caused by the movement of transposons. An extensive mutant screen was therefore conducted to identify Escherichia coli host factors that regulate transposition. An E. coli mutant library was screened using a papillation assay that allows detection of IS903 transposition events by the formation of blue papillae on a colony. Several host mutants were identified that exhibited a unique papillation pattern: a predominant ring of papillae just inside the edge of the colony, implying that transposition was triggered within these cells based on their spatial location within the colony. These mutants were found to be in pur genes, whose products are involved in the purine biosynthetic pathway. The transposition ring phenotype was also observed with Tn552, but not Tn10, establishing that this was not unique to IS903 and that it was not an artifact of the assay. Further genetic analyses of purine biosynthetic mutants indicated that the ring of transposition was consistent with a GTP requirement for IS903 and Tn552 transposition. Together, our observations suggest that transposition occurs during late stages of colony growth and that transposition occurs inside the colony edge in response to both a gradient of exogenous purines across the colony and the developmental stage of the cells.

The Local Sanarelli-Shwartzman Phenomenon in Rats Induced by Human Leukaemic Cells

1973 ◽  
Vol 29 (02) ◽  
pp. 353-362
Author(s):  
J Lisiewicz ◽  
A Pituch ◽  
J. A Litwin
Keyword(s):  
Chronic Lymphocytic Leukaemia ◽  
Intravenous Injection ◽  
Peripheral Blood ◽  
Lymphocytic Leukaemia ◽  
Acute Myeloblastic Leukaemia ◽  
Demarcation Line ◽  
E Coli ◽  
Leukaemic Cells ◽  
Shwartzman Phenomenon

SummaryThe local Sanarelli-Shwartzman phenomenon (SSP-L) in the skin of 30 rats was induced by an intr a cutaneous sensitizing injection of leukaemic leucocytes isolated from the peripheral blood of patients with chronic lymphocytic leukaemia (CLL), acute myeloblastic leukaemia (AL) and chronic granulocytic leukaemia (CGL) and challenged by an intravenous injection of 100(μ of E. coli endotoxin. SSP-L was observed in 7 rats after injection of CLL lymphocytes and in 6 and 2 rats after AL myeloblasts and the CGL granulocytes, respectively. The lesions in the skin after AL myeloblasts appeared in a shorter time and were of longer duration compared with those observed after CLL lymphocytes and CGL granulocytes. Histologically, the lesions consisted of areas of destruction in the superficial layers of the skin ; the demarcation line showed the presence of neutrophils, macrophages and erythrocytes. Haemorrhages and fibrin deposits near the demarcation line were larger after injection of CLL lymphocytes and AL myeloblasts than after CGL granulocytes. The possible role of leucocyte procoagulative substances in the differences observed have been discussed.

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