Hemocytometric characteristics of COVID-19 patients with and without cytokine Storm syndrome on the Sysmex XN-10 hematology analyzer

Author(s):  
Remy J. H. Martens ◽  
Arjan J. van Adrichem ◽  
Nadine J. A. Mattheij ◽  
Calvin G. Brouwer ◽  
Daan J. L. van Twist ◽  
...  

AbstractObjectivesCOVID-19 is an ongoing global pandemic. There is an urgent need for identification and understanding of clinical and laboratory parameters related to progression towards a severe and fatal form of this illness, often preceded by a so-called cytokine-storm syndrome (CSS). Therefore, we explored the hemocytometric characteristics of COVID-19 patients in relation to the deteriorating clinical condition CSS, using the Sysmex XN-10 hematology analyzer.MethodsFrom March 1st till May 16th, 2020, all patients admitted to our hospital with respiratory complaints and suspected for COVID-19 were included (n=1,140 of whom n=533 COVID-19 positive). The hemocytometric parameters of immunocompetent cells in peripheral blood (neutrophils [NE], lymphocytes [LY] and monocytes [MO]) obtained upon admission to the emergency department (ED) of COVID-19 positive patients were compared with those of the COVID-19 negative ones. Moreover, patients with CSS (n=169) were compared with COVID-19 positive patients without CSS, as well as with COVID-19 negative ones.ResultsIn addition to a significant reduction in leukocytes, thrombocytes and absolute neutrophils, it appeared that lymphocytes-forward scatter (LY-FSC), and reactive lymphocytes (RE-LYMPHO)/leukocytes were higher in COVID-19-positive than negative patients. At the moment of presentation, COVID-19 positive patients with CSS had different neutrophils-side fluorescence (NE-SFL), neutrophils-forward scatter (NE-FSC), LY-FSC, RE-LYMPHO/lymphocytes, antibody-synthesizing (AS)-LYMPHOs, high fluorescence lymphocytes (HFLC), MO-SSC, MO-SFL, and Reactive (RE)-MONOs. Finally, absolute eosinophils, basophils, lymphocytes, monocytes and MO-FSC were lower in patients with CSS.ConclusionsHemocytometric parameters indicative of changes in immunocompetent peripheral blood cells and measured at admission to the ED were associated with COVID-19 with and without CSS.

Author(s):  
Maksim Leonidovich Maksimov ◽  
Albina Ayratovna Zvegintseva ◽  
Lyudmila Yurievna Kulagina ◽  
Albina Zainutdinovna Nigmedzyanova ◽  
Elvina Ramisovna Kadyseva

A review article is based on current foreign sources. The level of cytokines in the peripheral blood can be increased in many diseases, but in some cases there may be an excess of their normal concentration in tens, hundreds or more times with the development of a peculiar clinical picture, which is based on a systemic inflammatory reaction. In the literature this condition has received the figurative name «cytokine storm», which highlights an extremely violent reaction of the immune system with an unknown (often unfavorable) outcome. Close attention of the scientific world and the public to the problem of extremely high levels of cytokines in the peripheral blood (hypercytokinemia) was drawn due to the high frequency of the cytokine storm in the novel coronavirus infection.


2020 ◽  
Vol 21 (4) ◽  
pp. 23-26
Author(s):  
A. Z. Aliyeva ◽  
◽  
A. E. Esedova ◽  
T. M. Dibirov ◽  
M. M. Bakayev ◽  
...  

Aim. To study the activity of myeloperoxidase in the peripheral blood of pregnant women in normal and thyroid diseases. Materials and methods. Cytochemical analysis was used to study the activity of myeloperoxidase in peripheral blood neutrophils of pregnant women with diffuse toxic goiter, as well as in women with the physiological course of pregnancy in a comparative aspect. Results. It was found that in women with a physiological course of pregnancy, the cytochemical parameters of myeloperoxidase in neutrophils were reduced only in the 1st trimester of pregnancy. In patients with diffuse toxic goiter, with severe thyrotoxicosis syndrome, the activity of the enzyme was significantly reduced during all periods of pregnancy. Apparently, these shifts of the enzyme, which is the main component of the protective system of blood phagocytes, are associated with their functional stress. Conclusion. Based on this opinion, it seems that blood neutrophils enter the system of thyroid hormone metabolism by their degradation. Apparently, this mechanism is activated with an increased content of hormones in the circulation, which occurs during pregnancy, and especially with concomitant diffuse toxic goiter with thyrotoxicosis syndrome and is aimed at preserving homeostasis necessary for normal fetal development.


Author(s):  
Lothar Thomas ◽  
Susanne Franck ◽  
Maren Messinger ◽  
Jo Linssen ◽  
Marcus Thomé ◽  
...  

AbstractThe aims of this study were to diagnose iron-restricted erythropoiesis (functional iron deficiency) in patients with classic iron deficiency (ID), anemia of chronic disease (ACD) and the combined state of ID/ACD with the use of two hematological methods for the measurement of reticulocyte hemoglobinization. In comparison, the biochemical markers of iron status were determined. We studied 474 anemic patients admitted to hospital with a broad spectrum of diseases. We measured indicators of reticulocyte hemoglobinization. CHr was determined on an Advia 120 hematology analyzer. A Sysmex XE-2100 hematology analyzer was used to determine RET-Y, the forward scatter of fluorescence-labeled reticulocytes, which can also be expressed as the reticulocyte hemoglobin equivalent (RET-H


mBio ◽  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tatiane S. Lima ◽  
Sharmila Mallya ◽  
Allen Jankeel ◽  
Ilhem Messaoudi ◽  
Melissa B. Lodoen

ABSTRACT Toxoplasma gondii is an intracellular protozoan parasite that has the remarkable ability to infect and replicate in neutrophils, immune cells with an arsenal of antimicrobial effector mechanisms. We report that T. gondii infection extends the life span of primary human peripheral blood neutrophils by delaying spontaneous apoptosis, serum starvation-induced apoptosis, and tumor necrosis alpha (TNF-α)-mediated apoptosis. T. gondii blockade of apoptosis was associated with an inhibition of processing and activation of the apoptotic caspases caspase-8 and -3, decreased phosphatidylserine exposure on the plasma membrane, and reduced cell death. We performed a global transcriptome analysis of T. gondii-infected peripheral blood neutrophils using RNA sequencing (RNA-Seq) and identified gene expression changes associated with DNA replication and DNA repair pathways, which in mature neutrophils are indicative of changes in regulators of cell survival. Consistent with the RNA-Seq data, T. gondii infection upregulated transcript and protein expression of PCNA, which is found in the cytosol of human neutrophils, where it functions as a key inhibitor of apoptotic pro-caspases. Infection of neutrophils resulted in increased interaction of PCNA with pro-caspase-3. Inhibition of this interaction with an AlkB homologue 2 PCNA-interacting motif (APIM) peptide reversed the infection-induced delay in cell death. Taken together, these findings indicate a novel strategy by which T. gondii manipulates cell life span in primary human neutrophils, which may allow the parasite to maintain an intracellular replicative niche and avoid immune clearance. IMPORTANCE Toxoplasma gondii is an obligate intracellular parasite that can cause life-threatening disease in immunocompromised individuals and in the developing fetus. Interestingly, T. gondii has evolved strategies to successfully manipulate the host immune system to establish a productive infection and evade host defense mechanisms. Although it is well documented that neutrophils are mobilized during acute T. gondii infection and infiltrate the site of infection, these cells can also be actively infected by T. gondii and serve as a replicative niche for the parasite. However, there is a limited understanding of the molecular processes occurring within T. gondii-infected neutrophils. This study reveals that T. gondii extends the life span of human neutrophils by inducing the expression of PCNA, which prevents activation of apoptotic caspases, thus delaying apoptosis. This strategy may allow the parasite to preserve its replicative intracellular niche.


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