scholarly journals STUDIES ON THE PATHOGENESIS OF ACUTE INFLAMMATION

1960 ◽  
Vol 111 (1) ◽  
pp. 45-64 ◽  
Author(s):  
Fred Allison ◽  
Margie G. Lancaster
Keyword(s):  
Blood Cells ◽  
Blood Clotting ◽  
Acute Inflammation ◽  
White Blood Cells ◽  
Blood Stream ◽  
Blood Levels ◽  
Primary Role ◽  
Low Levels

The relation of intravascular fibrin to the leucocytic sticking reaction in ear chambers of rabbits injured by heat was investigated in two ways. First, attempts were made to destroy the thin layer of fibrin believed to coat the surfaces of cells involved in the sticking reaction. Second, white cell sticking was studied after fibrinogen had been removed from the blood stream. The results of these experiments were as follows:— 1. Activation of fibrinolysin in vivo by streptokinase did not impair sticking of white blood cells. 2. Administration of streptokinase parenterally did not lower fibrinogen blood levels appreciably even when the amount used was large. 3. Thromboplastin infusions alone reduced circulating fibrinogen to low levels but leucocytic sticking was not prevented. Furthermore, frequent death of animals due to pulmonary embolism made such experiments prohibitive. 4. Addition of streptokinase to thromboplastin infusions protected against embolic deaths but did not influence sticking even though the fibrinogen levels achieved were quite low. 5. Finally, when thrombin was added to infusions of thromboplastin and streptokinase, no circulating fibrinogen could be detected. Under such circumstances leucocytic sticking following heat injury occurred without reduction. These findings were interpreted as evidence against a primary role of the blood clotting mechanism in causing the sticking of white blood cells to injured endothelium. Alternative explanations were discussed.

scholarly journals Bioavailability and Safety of Lipid Fraction from Different Taxa of Microalgae in Female C57BL/6 Mice

2021 ◽  
Vol 12 (5) ◽  
pp. 6845-6862
Keyword(s):  
Toxic Effect ◽  
Blood Cells ◽  
Cytokine Production ◽  
Lipid Fraction ◽  
White Blood Cells ◽  
Blood Levels ◽  
Proliferative Potential ◽  
Functional Activities ◽  
Acute Toxic Effect

Microalgae exhibit antioxidant, anti-inflammatory effects. In this study, we analyzed the toxicity of lipid fraction of different taxa of microalgae in female C57BL/6 mice. The number of red blood cells, white blood cells and subsets, hemoglobin, number, and functional activities of immature and mature immunocytes, biochemical parameters in blood serum, and kidney and liver extract were investigated. It is shown that the lipid fraction of microalgae had no acute toxic effect on body weight, glucose blood levels, and hemopoiesis in mice. Some changes in the number of immature and mature lymphocytes, proliferative potential, Ig levels, cytokine production were determined. In vivo lipid fraction of microalgae caused changes in cytokine, protein, lipid, purine, aminotransferases, and sex hormone level in mice. Obtained data indicate that lipid fraction dietary administration in female C57BL/6 mice does not have a toxic effect on the animal.

scholarly journals STUDIES ON THE PATHOGENESIS OF ACUTE INFLAMMATION

1961 ◽  
Vol 114 (4) ◽  
pp. 535-554 ◽  
Author(s):  
Fred Allison ◽  
Margie G. Lancaster
Keyword(s):  
Inflammatory Reaction ◽  
Vascular Endothelium ◽  
Blood Cells ◽  
Acute Inflammation ◽  
White Blood Cells ◽  
Unexpected Finding ◽  
Heparin Sodium ◽  
Rabbit Ear

Vigorous anticoagulation with heparin sodium and sodium warfarin singly and in combination did not prevent the margination and endothelial sticking reaction of leucocytes in rabbit ear chambers damaged by heat. The general inflammatory reaction observed in this preparation was similarly uninfluenced by the anticoagulants. An unexpected finding after administration of heparin was the enhanced formation of platelet and fibrin-like thrombi within damaged ear chambers. Sodium warfarin did not induce or prevent this heparin effect. Production of these heparin-associated thrombi was minimized in animals subjected to defibrinogenation in vivo whereas leucocytic sticking was not modified. Although defibrinogenation was not absolute, these experiments represent additional proof that the sticking of white blood cells to vascular endothelium is not causally related to the fibrinogen-fibrin system.

scholarly journals The Enigma of Eosinophil Degranulation

2021 ◽  
Vol 22 (13) ◽  
pp. 7091
Author(s):  
Timothée Fettrelet ◽  
Lea Gigon ◽  
Alexander Karaulov ◽  
Shida Yousefi ◽  
Hans-Uwe Simon
Keyword(s):  
Blood Cells ◽  
Inflammatory Diseases ◽  
White Blood Cells ◽  
Exact Role ◽  
Effector Cells ◽  
Effector Functions ◽  
Cytotoxic Effector ◽  
Eosinophil Degranulation

Eosinophils are specialized white blood cells, which are involved in the pathology of diverse allergic and nonallergic inflammatory diseases. Eosinophils are traditionally known as cytotoxic effector cells but have been suggested to additionally play a role in immunomodulation and maintenance of homeostasis. The exact role of these granule-containing leukocytes in health and diseases is still a matter of debate. Degranulation is one of the key effector functions of eosinophils in response to diverse stimuli. The different degranulation patterns occurring in eosinophils (piecemeal degranulation, exocytosis and cytolysis) have been extensively studied in the last few years. However, the exact mechanism of the diverse degranulation types remains unknown and is still under investigation. In this review, we focus on recent findings and highlight the diversity of stimulation and methods used to evaluate eosinophil degranulation.

scholarly journals Role of Calcium in Phosphatidylserine Externalisation in Red Blood Cells from Sickle Cell Patients

Anemia ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Erwin Weiss ◽  
David Charles Rees ◽  
John Stanley Gibson
Keyword(s):  
Red Blood Cells ◽  
Sickle Cell ◽  
Blood Cells ◽  
Phosphatidylserine Exposure ◽  
Channel Inhibition ◽  
Cation Conductance ◽  
Gardos Channel ◽  
Cation Permeability

Phosphatidylserine exposure occurs in red blood cells (RBCs) from sickle cell disease (SCD) patients and is increased by deoxygenation. The mechanisms responsible remain unclear. RBCs from SCD patients also have elevated cation permeability, and, in particular, a deoxygenation-induced cation conductance which mediates entry, providing an obvious link with phosphatidylserine exposure. The role of was investigated using FITC-labelled annexin. Results confirmed high phosphatidylserine exposure in RBCs from SCD patients increasing upon deoxygenation. When deoxygenated, phosphatidylserine exposure was further elevated as extracellular [] was increased. This effect was inhibited by dipyridamole, intracellular chelation, and Gardos channel inhibition. Phosphatidylserine exposure was reduced in high saline. levels required to elicit phosphatidylserine exposure were in the low micromolar range. Findings are consistent with entry through the deoxygenation-induced pathway (), activating the Gardos channel. [] required for phosphatidylserine scrambling are in the range achievablein vivo.

Candida albicans Shunt Infection: Report of Two Cases

Neurosurgery ◽  
1986 ◽  
Vol 19 (1) ◽  
pp. 111-113 ◽  
Author(s):  
David J. Gower ◽  
Kerry Crone ◽  
Eben Alexander ◽  
David L. Kelly
Keyword(s):  
Candida Albicans ◽  
Blood Cells ◽  
White Blood Cells ◽  
Shunt Infection ◽  
Cerebrospinal Fluid Shunts ◽  
Previous Therapy ◽  
Relationship Of ◽  
The Relationship ◽  
Overall Mortality

Abstract Infection of cerebrospinal fluid shunts with Candida albicans is reported in two patients. Scanning electron microscopy in one case demonstrates the relationship of the Candida hyphae to the white blood cells and to silicone plastic. A review of 10 previously reported cases of Candida shunt infection indicates that the infection usually follows a major bacterial infection or direct contamination or occurs spontaneously, Previous therapy has usually involved removal of the shunt, and the role of parenteral antifungal therapy is still unclear. Overall mortality to date is 25%.

scholarly journals Antagonists of the system L neutral amino acid transporter (LAT) promote endothelial adhesivity of human red blood cells

2017 ◽  
Vol 117 (07) ◽  
pp. 1402-1411 ◽  
Author(s):  
Laura Beth Mann Dosier ◽  
Vikram J. Premkumar ◽  
Hongmei Zhu ◽  
Izzet Akosman ◽  
Michael F. Wempe ◽  
...  
Keyword(s):  
Amino Acid ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Amino Acid Transporter ◽  
Neutral Amino Acid ◽  
Neutral Amino Acid Transporter ◽  
System L

SummaryThe system L neutral amino acid transporter (LAT; LAT1, LAT2, LAT3, or LAT4) has multiple functions in human biology, including the cellular import of S-nitrosothiols (SNOs), biologically active derivatives of nitric oxide (NO). SNO formation by haemoglobin within red blood cells (RBC) has been studied, but the conduit whereby a SNO leaves the RBC remains unidentified. Here we hypothesised that SNO export by RBCs may also depend on LAT activity, and investigated the role of RBC LAT in modulating SNO-sensitive RBC-endothelial cell (EC) adhesion. We used multiple pharmacologic inhibitors of LAT in vitro and in vivo to test the role of LAT in SNO export from RBCs and in thereby modulating RBC-EC adhesion. Inhibition of human RBC LAT by type-1-specific or nonspecific LAT antagonists increased RBC-endothelial adhesivity in vitro, and LAT inhibitors tended to increase post-transfusion RBC sequestration in the lung and decreased oxygenation in vivo. A LAT1-specific inhibitor attenuated SNO export from RBCs, and we demonstrated LAT1 in RBC membranes and LAT1 mRNA in reticulocytes. The proadhesive effects of inhibiting LAT1 could be overcome by supplemental L-CSNO (S-nitroso-L-cysteine), but not D-CSNO or L-Cys, and suggest a basal anti-adhesive role for stereospecific intercellular SNO transport. This study reveals for the first time a novel role of LAT1 in the export of SNOs from RBCs to prevent their adhesion to ECs. The findings have implications for the mechanisms of intercellular SNO signalling, and for thrombosis, sickle cell disease, and post-storage RBC transfusion, when RBC adhesivity is increased.

scholarly journals In-vivo Antiplasmodial Effect of Dihydroartemisinin-Piperaquine-Nitrofurantoin on Plasmodium berghei- Infected Mice

2021 ◽  
pp. 12-20
Author(s):  
Udeme O. Georgewill ◽  
Festus Azibanigha Joseph ◽  
Elias Adikwu
Keyword(s):  
Plasmodium Berghei ◽  
Blood Cells ◽  
Hematological Parameters ◽  
White Blood Cells ◽  
Positive Control ◽  
Negative Control ◽  
Antiplasmodial Activity ◽  
Significant Difference ◽  
Tract Infections

Nitrofurantoin (NT) used for the treatment of urinary tract infections may have antiplasmodial activity. Dihydroartemisinin-piperaquine (DP) is an artemisinin based combination therapy used for the treatment of malaria. This study evaluated the antiplasmodial effect of dihydroartemisinin-piperaquine-nitrofurantoin (DP-NT) on mice infected with Plasmodium berghei. Adult Swiss albino mice (30-35 g) of both sexes were used. The mice were randomly grouped, inoculated with Plasmodium berghei, and treated orally with DP (1.7/13.7 mg/kg), NT (57.1 mg/kg) and DP-NT (1.71/13.7/ 57.1 mg/kg), respectively using curative, prophylactic and suppressive tests. The negative control was orally treated with normal saline (0.3 mL), while the positive control was orally treated with chloroquine CQ (10mg/kg). After treatment, blood samples were collected and evaluated for percentage parasitemia, inhibitions and hematological parameters. Liver samples were evaluated for histological changes. The mice were observed for mean survival time (MST). Treatment with DP-NT decreased parasitemia levels when compared to individual doses of DP and NT with significant difference observed at p<0.05. DP-NT prolonged MST when compared to individual doses of DP and NT with significant difference observed at p<0.05. The decrease in packed cell volume, red blood cells, hemoglobin and increase in white blood cells in parasitized mice were significantly restored by DP-NT  when compared to individual doses of DP and NT with difference observed at p<0.05. DP-NT eradicated liver Plasmodium parasite.  NT remarkably increased the antiplasmodial activity of DP. DP-NT may be used for the treatment of malaria.

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