scholarly journals The Effect of Lithium Chloride on Neutrophil Activation on Exposure to Serum of Patients with Septic Shock

2020 ◽  
Vol 16 (5) ◽  
pp. 45-55
Author(s):  
O. A. Grebenchikov ◽  
I. S. Kasatkina ◽  
K. K. Kadantseva ◽  
M. A. Meshkov ◽  
A. A. Bayeva

The aim of the study: to examine the anti-inflammatory effect of lithium chloride by exposing the human neutrophils to serum of patients with septic shock in vitro.Material and methods. The study was carried out on neutrophils extracted from the blood of 6 healthy donors, which were activated with serum from patients with septic shock. The neutrophil activity was evaluated with fluorescent antibodies to the CD11b and CD66b markers of degranulation. The level of human neutrophil apoptosis and necrosis was assessed 22 hours after extraction; quantitative assessment was made using annexin V and propidium iodide with flow cytofluorimetry. Intact and activated neutrophils were treated with 0.3, 3.0 and 9.0 mmol lithium chloride solution.Results. The level of CD11b expression on the surface of intact neutrophils (healthy donors) was 3434.50 [3311.0-3799.0] arbitrary fluorescence units (AFU). Incubation of neutrophils with serum of patients with septic shock increased CD11b expression 2.5 times to 8589.0 [7279.0-11258.0] AFU (P=0.005) vs intact leukocytes, and increased CD66b expression 2.7 times up to 27 600.0 [22 999.0-28 989.0] AFU ((P=0.005) vs intact neutrophils. Lithium chloride in concentrations of 0.3, 3.0 and 9.0 mmol in a dose-dependent manner reduced the level of expression of CD11b and CD66b molecules on the surface of activated neutrophils. Septic serum reduced spontaneous neutrophil apoptosis, and 3.0 mmol and higher lithium chloride solution induced spontaneous neutrophil apoptosis.Conclusion. Lithium chloride reduces the activation of neutrophils preactivated by serum of patients with septic shock, reduces expression of CD11b and CD66b molecules on the neutrophil surface, inhibiting the process of their activation (degranulation). Lithium chloride in concentration of 3.0 mmol and higher is able to induce spontaneous apoptosis of neutrophils activated by serum of patients with septic shock.

2019 ◽  
Vol 22 (suppl 1) ◽  
Author(s):  
Stephania Cappellari de Rezende ◽  
Isabela Dainezi ◽  
Raíra Chefer Apolinario ◽  
Lucíola Lucena de Sousa ◽  
Neide Aparecida Mariano

Blood ◽  
1998 ◽  
Vol 92 (12) ◽  
pp. 4808-4818 ◽  
Author(s):  
Bengt Fadeel ◽  
Anders Åhlin ◽  
Jan-Inge Henter ◽  
Sten Orrenius ◽  
Mark B. Hampton

Abstract Human neutrophils have a short half-life and are believed to die by apoptosis or programmed cell death both in vivo and in vitro. We found that caspases are activated in a time-dependent manner in neutrophils undergoing spontaneous apoptosis, concomitant with other characteristic features of apoptotic cell death such as morphologic changes, phosphatidylserine (PS) exposure, and DNA fragmentation. The treatment of neutrophils with agonistic anti-Fas monoclonal antibodies (MoAbs) significantly accelerated this process. However, in cells treated with the potent neutrophil activator phorbol 12-myristate 13-acetate (PMA), caspase activity was only evident after pharmacologic inhibition of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Similarily, inhibition of the NADPH oxidase in constitutive and Fas/APO-1–triggered apoptosis resulted in increased rather than suppressed levels of caspase activity, suggesting that reactive oxygen species may prevent caspases from functioning optimally in these cells. Moreover, oxidants generated via the NADPH oxidase were essential for PS exposure during PMA-induced cell death, but not for neutrophils undergoing spontaneous apoptosis. We conclude that caspases are an important component of constitutive and Fas/APO-1–triggered neutrophil apoptosis. However, these redox sensitive enzymes are suppressed in activated neutrophils, and an alternate oxidant-dependent pathway is used to mediate PS exposure and neutrophil clearance under these conditions.


1993 ◽  
Vol 97 (41) ◽  
pp. 10835-10839 ◽  
Author(s):  
Koji Yamanaka ◽  
Motoyuki Yamagami ◽  
Toshiyuki Takamuku ◽  
Toshio Yamaguchi ◽  
Hisanobu Wakita

Blood ◽  
2019 ◽  
Vol 133 (20) ◽  
pp. 2186-2197 ◽  
Author(s):  
Denis F. Noubouossie ◽  
Brandi N. Reeves ◽  
Brian D. Strahl ◽  
Nigel S. Key

Abstract Reactive and clonal neutrophil expansion has been associated with thrombosis, suggesting that neutrophils play a role in this process. However, although there is no doubt that activated monocytes trigger coagulation in a tissue factor-dependent manner, it remains uncertain whether stimulated neutrophils can also directly activate coagulation. After more than a decade of debate, it is now largely accepted that normal human neutrophils do not synthetize tissue factor, the initiator of the extrinsic pathway of coagulation. However, neutrophils may passively acquire tissue factor from monocytes. Recently, the contact system, which initiates coagulation via the intrinsic pathway, has been implicated in the pathogenesis of thrombosis. After the recent description of neutrophil extracellular trap (NET) release by activated neutrophils, some animal models of thrombosis have demonstrated that coagulation may be enhanced by direct NET-dependent activation of the contact system. However, there is currently no consensus on how to assess or quantify NETosis in vivo, and other experimental animal models have failed to demonstrate a role for neutrophils in thrombogenesis. Nevertheless, it is likely that NETs can serve to localize other circulating coagulation components and can also promote vessel occlusion independent of fibrin formation. This article provides a critical appraisal of the possible roles of neutrophils in thrombosis and highlights some existing knowledge gaps regarding the procoagulant activities of neutrophil-derived extracellular chromatin and its molecular components. A better understanding of these mechanisms could guide future approaches to prevent and/or treat thrombosis.


Author(s):  
A A Al-Farayedhi ◽  
P Gandhidasan ◽  
M A Antar ◽  
M S Abdul Gaffar

This article presents the results of an experimental study on the performance of a structured packing dehumidifier and the regenerator system. The system is tested using different proportions of an aqueous desiccant mixture of calcium chloride and lithium chloride solutions with an overall concentration of 40 wt%. The instantaneous effectiveness and the time-average effectiveness of the dehumidification process as well as the regeneration process are defined for the hybrid cooling system. It is found that as the lithium chloride content in the solution increases, the effectiveness of the dehumidifier as well as the regenerator increases. Moreover, the regeneration of the lithium chloride solution is found to be more effective than that of calcium chloride solution. The dehumidifier effectiveness using the desiccant mixture of 20 wt% CaCl2 and 20 wt% LiCl is found to be close to that of 45 wt% solution of calcium chloride and improves by ɛ80 per cent over the 40 wt% solution of calcium chloride.


1964 ◽  
Vol 42 (5) ◽  
pp. 575-581 ◽  
Author(s):  
H. L. A. Tarr

Soluble extracts of immature sockeye salmon milts were prepared by blending them with 0.66 M lithium chloride solution to effect plasmolysis, followed by dilution to 0.10 M concentration with water and removal of the precipitated nucleoprotamine by centrifuging. By means of radioactive tracer technique it was shown that these extracts phosphorylated adenine, guanine, hypoxanthine, thymine, uracil, cytosine, and orotic acid in the presence of α-phosphoribosylpyrophosphate to yield ribomononucleotides.


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