scholarly journals THE IMPACT OF ELECTROMAGNETIC RADIATION OF MOBILE PHONE FOR LYMPHOCYTE ACTIVATION IN VITRO

2019 ◽  
Vol 96 (10) ◽  
pp. 965-970 ◽  
Author(s):  
Maria S. Blyakher ◽  
E. A. Tulskaya ◽  
I. V. Kapustin ◽  
I. M. Fedorova ◽  
T. K. Lopatina ◽  
...  
Keyword(s):  
Electromagnetic Radiation ◽  
Mobile Phone ◽  
Blood Cells ◽  
Cytokine Production ◽  
Venous Blood ◽  
Peripheral Blood Lymphocytes ◽  
Mean Values ◽  
Healthy Donors ◽  
The Impact

The character of the influence of the electromagnetic radiation (EMR) of mobile phone on the activation of lymphocytes in vitro was investigated. This is important, since modern human is exposed to a complex combination of electric and magnetic fields (EMF) of different frequencies. The object of the study were whole venous blood and lymphocytes isolated from 21 adult donors (aged of from 20 to 55 years) - 10 were healthy donors and 11 were healthy persons 7 days after their vaccination with meningococcal polysaccharide vaccine. In the study the influence of phone’s EMR on the functional activity of peripheral blood lymphocytes was determined by the flow cytometry method with the use of monoclonal antibodies of Beckman Coulter company (by the identification and calculation the number of basic and activated lymphocyte subpopulations). The changes of cytokines production by blood cells exposed to mobile phone electromagnetic radiation were determined in supernatants by measuring their concentration using EIA kits produced by JSC “Vector-Best” (Russia) and LLC “cytokine” (Russia). The results of the study of the effects of electromagnetic radiation of mobile phone on blood cells revealed changes in the percentage of lymphocytes carrying the early activation marker CD69 significantly to be more frequently and were observed with greater intensity in the group of donors which were vaccinated compared to healthy donors. Under the influence of phone’s EMR mean values of cytokine production determined in the supernatants samples did not changed in both groups, but in the group of healthy donors mean values of cytokines production were 1,5 - 2 times higher than in the group of persons following immunization. The increase or decrease in cytokine production under the influence of phone’s EMR occurred regardless of the initial level of its production in the surveyed donor. The changes of the cytokine production (IFNγ, TNFα, IL-6 and IL-8) by blood cells under the influence of phone’s EMR happen individually; this should be considered when deciding on the presence or absence of phone’s EMR impact on the status of lymphocytes.

scholarly journals LAG3 is a Central Regulator of NK Cell Cytokine Production

2020 ◽  
Author(s):  
Sriram Narayanan ◽  
Patricia J. Ahl ◽  
Veonice Au Bijin ◽  
Nivashini Kaliaperumal ◽  
Seng Gee Lim ◽  
...  
Keyword(s):  
Nk Cells ◽  
Cytokine Production ◽  
Viral Infections ◽  
Nk Cell ◽  
Chronic Viral Hepatitis ◽  
Negative Regulator ◽  
Surface Receptors ◽  
Healthy Donors ◽  
The Impact

AbstractNatural killer (NK) cells are innate effectors, which play a crucial role in controlling viral infections. Administration of IFN-α has shown promising results as a therapeutic, controlling HIV, and chronic viral hepatitis. However the downstream mechanisms by which IFN-α mediates its anti-viral effects is largely unknown. In this investigation, we evaluated the impact of IFN-α on peripheral blood NK cells from healthy donors. High dimensional flow cytometry analysis of NK cell surface receptors following exposure to IFN-α showed an increased expression of the check point inhibitor LAG3. Further characterization revealed that LAG3 was expressed in a subset of NK cells with high expression of activation and maturation markers. Assessment of metabolic pathways showed that LAG3+ NK cells had enhanced rates of glycolysis and glycolytic capacity, suggesting that it is a primed effector subset with enhanced glucose metabolism. Inhibition of LAG3 on NK cells using antibody in vitro resulted in a profound increase in secretion of cytokines IFN-γ, TNF-α, MIP-1α and MIP-1β, without affecting the cytotoxic activity. Taken together, these results showed that LAG3 is a negative regulator of cytokine production by mature NK cells.

scholarly journals Impact of a cellphone electromagnetic radiation on phagocytic activity of neutrophils in vitro

2020 ◽  
Vol 99 (9) ◽  
pp. 925-929
Author(s):  
Maria S. Blyakher ◽  
Elena A. Tulskaya ◽  
Ivan V. Kapustin ◽  
Irina M. Fedorova ◽  
Vladimir G. Nesterenko ◽  
...  
Keyword(s):  
Electromagnetic Radiation ◽  
Human Body ◽  
Mobile Communications ◽  
Phagocytic Activity ◽  
Venous Blood ◽  
Enzyme Linked Immunosorbent Assay ◽  
Physiological Processes ◽  
Immunological Tests ◽  
The Impact

Introduction. The nature of a cellphone electromagnetic radiation (EMP) influence on the neutrophils in vitro activation was studied. The relevance of studying the impact of mobile communications and their effects on the body’s physiological processes is determined by the global prevalence of such tools and the research data inconsistency in the both domestic and foreign scientific literature. Material and methods. The object of the study was the whole venous blood samples and isolated neutrophils from 36 adult donors (aged from 22 to 65 years) of both genders. The responses of the neutrophils’ phagocytic activity and its registration were carried out in a flat-bottomed plate for enzyme-linked immunosorbent assay (ELISA), the daily culture of S. aureus ATCC 6538 (strain 209) was used as an inducer of phagocytosis. The intensity of phagocytosis was evaluated by changing the activity of myeloperoxidase (MPO) spectrophotometric method in our modification. Results. In the course of studies of the EMR impact of a cellphone on phagocytic neutrophils, the following was revealed: when culturing neutrophils without the addition of S. aureus, there was a tendency to increase spontaneous MPO activity (by 69%), i.e. its production in the absence of a stimulating factor and, conversely, a significant decrease in the enzyme activity induced by S. aureus (by 34%, p <0.05), i.e. the phagocytic activity of neutrophils. Conclusion We revealed the biological effect of the cellphone EMR as an increase in the spontaneous activity of MPO and a decrease in the bacterially induced activity of the enzyme may indicate a decline in the phagocytic activity of the main cells of the immune system, therefore, it demonstrates a weakening of the protective properties of the human body against infectious diseases. In previous studies, we have shown the presence of the impact of cellphone EMR on the activation of lymphocytes in vitro. The use of immunological tests can be a promising direction in assessing the impact of the cellphone EMR on the human body.

scholarly journals Keratinocytes Regulate the Threshold of Inflammation by Inhibiting T Cell Effector Functions

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1606
Author(s):  
Peter Seiringer ◽  
Stefanie Eyerich ◽  
Kilian Eyerich ◽  
Daniela Dittlein ◽  
Anna Caroline Pilz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Cytokine Production ◽  
Nickel Sulfate ◽  
Human Keratinocytes ◽  
T Cell Proliferation ◽  
Effector Functions ◽  
The Impact ◽  
Cell Effector

Whilst the importance of keratinocytes as a first-line defense has been widely investigated, little is known about their interactions with non-resident immune cells. In this study, the impact of human keratinocytes on T cell effector functions was analyzed in an antigen-specific in vitro model of allergic contact dermatitis (ACD) to nickel sulfate. Keratinocytes partially inhibited T cell proliferation and cytokine production. This effect was dependent on the keratinocyte/T cell ratio and was partially reversible by increasing the number of autologous dendritic cells. The inhibition of T cell proliferation by keratinocytes was independent of the T cell subtype and antigen presentation by different professional antigen-presenting cells. Autologous and heterologous keratinocytes showed comparable effects, while the fixation of keratinocytes with paraformaldehyde abrogated the immunosuppressive effect. The separation of keratinocytes and T cells by a transwell chamber, as well as a cell-free keratinocyte supernatant, inhibited T cell effector functions to the same amount as directly co-cultured keratinocytes, thus proving that soluble factor/s account for the observed suppressive effects. In conclusion, keratinocytes critically control the threshold of inflammatory processes in the skin by inhibiting T cell proliferation and cytokine production.

scholarly journals Interferon beta-1a induces expression of brain-derived neurotrophic factor in human T lymphocytes in vitro and not in vivo

2020 ◽  
Vol 15 (1) ◽  
pp. FNL38 ◽  
Author(s):  
Zarlascht Karmand ◽  
Hans-Peter Hartung ◽  
Oliver Neuhaus
Keyword(s):  
T Cell ◽  
Neurotrophic Factor ◽  
Serum Levels ◽  
Brain Derived Neurotrophic Factor ◽  
Peripheral Blood Lymphocytes ◽  
T Cell Proliferation ◽  
Bdnf Expression ◽  
Healthy Donors

Aim: To detect IFN β-1a-induced expression of brain-derived neurotrophic factor (BDNF) to undermine the hypothesis of IFN β-1a-associated neuroprotection in multiple sclerosis (MS). Methods: The influence of IFN β-1a on in vitro activated peripheral blood lymphocytes from healthy donors was tested. Proliferation analyses were made to detect T-cell growth. BDNF expression was measured by standard ELISA. To assess the influence of IFN β-1a on BDNF expression in vivo, BDNF serum levels of MS patients treated with IFN β-1a were compared with those of untreated patients. Results: IFN β-1a inhibited T-cell proliferation dose dependently. It induced BDNF expression at middle concentrations. MS patients treated with IFN β-1a exhibited significantly lower BDNF serum levels than untreated patients. Conclusion: IFN β-1a may promote neuroprotection by inducing BDNF expression, but its importance in vivo remains open.

scholarly journals An endothelialized urothelial cell-seeded tubular graft for urethral replacement

2013 ◽  
Vol 7 (1-2) ◽  
pp. 4 ◽  
Author(s):  
Annie Imbeault ◽  
Geneviève Bernard ◽  
Alexandre Rousseau ◽  
Amélie Morissette ◽  
Stéphane Chabaud ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Cells ◽  
Human Fibroblasts ◽  
Surgical Techniques ◽  
Urethral Reconstruction ◽  
Full Thickness ◽  
Urothelial Cells ◽  
The Impact ◽  
Histology And Immunohistochemistry

Introduction: Many efforts are used to improve surgical techniques and graft materials for urethral reconstruction. We developed an endothelialized tubular structure for urethral reconstruction.Methods: Two tubular models were created in vitro. Human fibroblasts were cultured for 4 weeks to form fibroblast sheets. Then, endothelial cells (ECs) were seeded on the fibroblast sheets and wrapped around a tubular support to form a cylinder for the endothelialized tubular urethral model (ET). No ECs were added in the standard tubular model (T). After 21 days of maturation, urothelial cells were seeded into the lumen of both models. Constructs were placed under perfusion in a bioreactor for 1 week. At several times,histology and immunohistochemistry were performed on grafted nude mice to evaluate the impact of ECs on vascularization.Results: Both models produced an extracellular matrix, without exogenous material, and developed a pseudostratified urothelium. Seven days after the graft, mouse red blood cells were present only in the outer layers in T model, but in the full thickness of ET model. After 14 days, erythrocytes were present in both models, but in a greater proportion in ET model. At day 28, both models were well-vascularized, with capillary-like structures in the wholethickness of the tubes.Conclusion: Incorporating endothelial cells was associated with an earlier vascularization of the grafts, which could decrease the necrosis of the transplanted tissue. As those models can be elaborated with the patient’s cells, this tubular urethral graft would be unique in its autologous property.

scholarly journals Antagonistic Effects of CAPE (a Component of Propolis) on the Cytotoxicity and Genotoxicity of Irinotecan and SN38 in Human Gastrointestinal Cancer Cells In Vitro

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 658 ◽  
Author(s):  
Gabriela Gajek ◽  
Beata Marciniak ◽  
Jarosław Lewkowski ◽  
Renata Kontek
Keyword(s):  
Peripheral Blood ◽  
Human Peripheral Blood ◽  
Caffeic Acid Phenethyl Ester ◽  
Peripheral Blood Lymphocytes ◽  
Neoplastic Cells ◽  
Blood Lymphocytes ◽  
Human Peripheral Blood Lymphocytes ◽  
Apoptotic Activity ◽  
The Impact

The incidence of gastrointestinal cancers is increasing every year. Irinotecan (CPT-11), a drug used in the treatment of colorectal cancer and gastric cancer, is metabolized by carboxylesterases to an active metabolite, SN-38, which is more cytotoxic. CAPE (caffeic acid phenethyl ester) is an active component of propolis, which has a high antibacterial, antiviral, and antineoplastic potential. This study analyses the impact of CAPE on the cytotoxic (MTT assay), genotoxic (comet assay) and proapoptotic (caspase-3/7 activity) potential of irinotecan and its metabolite SN-38 in cultures of gastrointestinal neoplastic cells (HCT116, HT29, AGS). Cytotoxicity and genotoxicity activities of these compounds were carried out in comparison with human peripheral blood lymphocytes (PBLs) in vitro. The antioxidant potential of CAPE was investigated in relation H2O2-induced oxidative stress in the both neoplastic cells and PBLs. CAPE expressed cytotoxic, genotoxic, and pro-apoptotic activity against AGS, HCT116, and HT29 tumor cells. CAPE, in the presence of different concentrations of irinotecan or SN38, decreased the cytotoxicity, genotoxicity, and pro-apoptotic activity in these cell lines, but it has no such action on normal human peripheral blood lymphocytes.

Comparison between Progenitor Cells from Mobilized Peripheral Blood (PB) in Healthy Donors and Non-Hodgkin’s Lymphoma (NHL) Patients.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 5002-5002
Author(s):  
Eva M. Villaron ◽  
Julia Almeida ◽  
Natalia Lopez-Holgado ◽  
Fermin M. Sanchez-Guijo ◽  
Mercedes Alberca ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Functional Assays ◽  
Healthy Donors ◽  
Cd34 Cells ◽  
Cell Subpopulations ◽  
The Impact ◽  
Pbsc Mobilization

Abstract INTRODUCTION: Peripheral blood stem cell (PBSC) mobilization is impaired in patients receiving chemotherapy but, as far as we know there is no data about the impact of chemotherapy on different PB progenitor cell subpopulations. AIM: to ascertain whether or not immature or committed progenitor cell are affected by chemotherapy prior PBSC mobilization in NHL patients. MATERIAL AND METHODS: a total of 27 PB samples from NHL patients and 36 PB samples from healthy donors were studied. Immunophenotypic analysis of CD34+ cell subpopulations was performed using the following four colour combinations of monoclonal antibodies (FITC/PE/PC5/APC): CD90/CD133/CD38/CD34 and CD71/CD13/CD45/CD34. In order to study committed progenitor cells “in vitro”, standard colony-forming assays were used and, in order to investigate the behaviour of the uncommitted progenitors Delta Assays of plastic adherent progenitor cells (PΔ) were performed. RESULTS: The comparison between NHL patients and healthy donors is shown in Table 1. The relationship between data obtained by flow cytometry and cultures was statistically significant (p<0.05, r>0.568) for all the progenitors analysed. Table 1: Results of Immunophenotypic and Functional Assays LNH patients Healthy donors p Data expressed as median (range). 1. Percentage among CD34+ cells. 2. Number of CFU/10 5 planted cells. 3. Number of CFU/10 6 planted cells % CD34 0.16(0.04–3.65) 0.57(0.11–1.81) 0.013 Immunophenotypic Data Erithroid 1 0.05(0.01–0.60) 0.14(0.02–0.42) 0.098 Myelo–monocytic 1 0.11(0.02–2.41) 0.37(0.07–1.18) 0.014 Immature 1 0.01(0.00–0.63) 0.05(0.01–0.19) 0.014 CFU-GM 2 70(4–440) 90(0–904) 0.327 Clonogenic and Delta Assays data BFU-E 2 62(6–172) 85(0–240) 0.046 CFU-Mix 2 18(0–124) 42(0–140) 0.018 CFU Δ3 356(0–3509) 953(90–8320) 0.033 CONCLUSIONS: We can conclude that in NHL, mobilized committed and above all immature progenitors are impaired when compared with healthy subjects, both analysed by immunological and functional assays. Only granulomonocytic progenitors analysed by a functional approach seemed to be preserved.

scholarly journals Targeting the Inflammatory Niche in MDS By Tasquinimod Restores Hematopoietic Support and Suppresses Immune-Checkpoint Expression in Vitro

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2596-2596
Author(s):  
Manja Wobus ◽  
Ekaterina Balaian ◽  
Uta Oelschlaegel ◽  
Russell Towers ◽  
Kristin Möbus ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mrna Expression ◽  
Immunohistochemical Staining ◽  
Research Funding ◽  
Fold Increase ◽  
Low Risk ◽  
Hematopoietic Stem ◽  
Healthy Donors ◽  
The Impact

Abstract Introduction Myelodysplastic syndromes (MDS) belong to the most common hematological neoplasms in the elderly population, characterized by ineffective hematopoiesis, peripheral cytopenia and the risk of transformation into acute myeloid leukemia. There is increasing evidence that an aberrant innate immune response and a proinflammatory bone marrow (BM) microenvironment play a critical role in the pathogenesis of MDS. The alarmin S100A9, a key player for regulation of inflammatory responses, has been shown to be elevated in MDS patients. It directs an inflammatory cell death (pyroptosis) by increased NF-kB mediated transcription and secretion of proinflammatory, hematopoiesis-inhibitory cytokines and production of reactive oxygen species. Tasquinimod (TASQ, Active Biotech) is a novel, oral small molecular drug with S100A9 inhibitory activity and it is currently investigated in a phase Ib/IIa trial in relapsed/refractory multiple myeloma (NCT04405167). TASQ has demonstrated anti-angiogenic, antitumor and immunomodulatory properties in a broad range of preclinical solid tumor models; however, little is known about its effects in myeloid malignancies. Aim We investigated the role of S100A9 in cellular models of MDS and the potential of TASQ to target S100A9 within the MDS stroma in vitro. Methods Immunohistochemical staining of S100A9, CD271+ mesenchymal stromal cells (MSCs), CD68+ macrophages and CD66b+ neutrophils in BM tissues from MDS patients and healthy donors was performed with multiplex immunohistochemistry and analyzed with the VECTRA imaging system. MSCs from patients with either low-risk MDS, CMML or age-adjusted healthy donors were exposed to S100A9 (1.5µg/ml) in the presence or absence of TASQ (10µM). Subsequently, TLR4 downstreaming molecules such as IRAK1, gasdermin and NF-kB-p65 were analyzed by Western blot. Moreover, the mRNA expression of further proinflammatory molecules (IL-1b, IL-18, caspase1) and PD-L1 was quantified by real-time PCR. To study the impact on the hematopoietic support, MSCs were pre-treated for one week with S100A9 ± TASQ before CD34+ hematopoietic stem and progenitor cells (HSPCs) were seeded on the stromal layer. The colony formation (CAF-C) was analyzed weekly followed by a CFU-GEMM assay in methylcellulose medium. Additionally, PD-1 mRNA expression was quantified in cocultured HSPCs. Results Immunohistochemical staining of BM tissue demonstrated S100A9 expression mainly by CD66b+ neutrophils and with less extent by CD68+ macrophages. In line with this, we could not detect relevant S100A9 mRNA expression in cultured MDS or healthy MSCs in vitro. Exposure of MDS and healthy MSCs with S100A9 induced TLR4 downstream signalling as demonstrated by increased expression of IRAK1 and NF-kB-p65. We further detected a higher expression of gasdermin, an inductor of pyroptosis, in S100A9 exposed MSCs. Addition of TASQ abolished these effects and inhibited the expression of the mentioned proteins, indicating an alleviation of inflammation. Furthermore, we detected a 2-fold increase of mRNA expression of the proinflammatory cytokines IL-1b and IL-18 as well as a 5-fold increase of their activator caspase 1 in MSCs after treatment with S100A9, which could be prevented by TASQ. Interestingly, PD-L1 as a potential downstream target was induced by S100A9 by 2.5-fold and could be suppressed by TASQ to about 50%. To evaluate the impact on the hematopoietic support of MSCs, we analysed MSC/HSPC cocultures after treatment with S100A9. We observed a decreased number of cobblestone area forming cells (CAF-C) as well as reduced numbers of colonies (CFU) in a subsequent clonogenic assay, indicating a disturbed hematopoietic support by S100A9 treated MSCs. Interestingly, both the number of CAF-C and CFU could be increased by TASQ pre-treatment. Finally, the PD-1 expression in co-cultured HSPCs was regulated in the same way as its ligand in treated MSCs, nominating this interaction as a potential target of S100A9/TASQ in the MDS BM. Conclusion In summary, we provide evidence that the pathological inflammasome activation in the myelodysplastic bone marrow can be rescued by TASQ at least in part by inhibition of the S100A9 mediated TLR4 downstream signalling including NF-kB-p65 transcription and PD-L1 expression. These effects result in an improved hematopoietic support by MSCs, suggesting a potential efficacy to improve cytopenia in low-risk MDS patients. Disclosures Balaian: Novartis: Honoraria. Törngren: Active Biotech: Current Employment. Eriksson: Active Biotech: Current Employment. Platzbecker: AbbVie: Honoraria; Takeda: Honoraria; Celgene/BMS: Honoraria; Novartis: Honoraria; Janssen: Honoraria; Geron: Honoraria. Röllig: Novartis: Honoraria, Research Funding; Jazz: Honoraria; Janssen: Honoraria; Bristol-Meyer-Squibb: Honoraria, Research Funding; Amgen: Honoraria; AbbVie: Honoraria, Research Funding; Pfizer: Honoraria, Research Funding; Roche: Honoraria, Research Funding.

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