Immunomodulatory Effects of Jacalin, A Dietary Plant Lectin on the Peripheral Blood Mononuclear Cells (PBMCs)

2021 ◽  
Author(s):  
Lavanya V ◽  
Anil Kumar Bommanabonia ◽  
Neesar Ahmed ◽  
Shazia Jamal
Keyword(s):  
Tumor Growth ◽  
Peripheral Blood Mononuclear Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Inflammatory Cytokine ◽  
Mononuclear Cells ◽  
Point Interaction ◽  
Peripheral Blood Mononuclear ◽  
Effector Cells ◽  
Blood Mononuclear Cells

Abstract The tumor microenvironment that refers to the tumour’s surroundings is a key modulator of tumor growth and invasion. The tumour derived signals are known to downregulate the anti-tumor effects of the effector cells present in the TME. Thus, the cross talk between the tumor cells with the surrounding immune cells helps in evading the tumor surveillance as well as aiding in tumor growth and proliferation. Hence, knowledge regarding the effects of drugs/compound on the tumor-stromal interactions are gaining importance. In the present study, the effects of jacalin, a dietary lectin on the proliferation and cytokine production of peripheral blood mononuclear cells (PBMCs) are investigated. Jacalin was shown to act as a mitogen of PBMCs, the key cytokine secreting immune cells. Also, jacalin initially induces increased mRNA expression of pro-inflammatory cytokine IFN-γ; however prolonged stimulation of PBMCs resulted in increased expression of anti-inflammatory cytokine, mainly TGF-β. Further, 6 h jacalin prestimulated PBMCs (Jac-PBMCs) were shown to inhibit HeLa cell proliferation while 24 h (Jac-PBMCs) were found to favor tumor growth. Thus, it may be postulated that while jacalin initially polarizes the PBMCs to hinder the tumor growth, after a stipulated time point, interaction of jacalin with PBMCs can lead to an immunosuppressive TME that may probably assist in tumor growth and progression.

scholarly journals Statin-induced microRNAome alterations modulating inflammation pathways of peripheral blood mononuclear cells in patients with hypercholesterolemia

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Hung-Ju Lin ◽  
Sung-Liang Yu ◽  
Ta-Chen Su ◽  
Hsiu-Ching Hsu ◽  
Ming-Fong Chen ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Quantitative Polymerase Chain Reaction ◽  
Density Lipoprotein ◽  
Cardiovascular Risks ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Abstract Statins inhibit cholesterol biogenesis and modulate atheroma inflammation to reduce cardiovascular risks. Promoted by immune and non-immune cells, serum C-reactive protein (CRP) might be a biomarker suboptimal to assess inflammation status. Although it has been reported that statins modulated inflammation via microRNAs (miRNAs), evidence remains lacking on comprehensive profiling of statin-induced miRNAome alterations in immune cells. We recruited 19 hypercholesterolemic patients receiving 2 mg/day pitavastatin and 15 ones receiving 10 mg/day atorvastatin treatment for 12 weeks, and performed microarray-based profiling of 1733 human mature miRNAs in peripheral blood mononuclear cells (PBMCs) before and after statin treatment. Differentially expressed miRNAs were determined if their fold changes were >1.50 or <0.67, after validated using quantitative polymerase chain reaction (qPCR). The miRSystem and miTALOS platforms were utilized for pathway analysis. Of the 34 patients aged 63.7 ± 6.2 years, 27 were male and 19 were with coronary artery disease. We discovered that statins induced differential expressions of miR-483-5p, miR-4667-5p, miR-1244, and miR-3609, with qPCR-validated fold changes of 1.74 (95% confidence interval, 1.33–2.15), 1.61 (1.25–1.98), 1.61 (1.01–2.21), and 1.68 (1.19–2.17), respectively. The fold changes of the four miRNAs were not correlated with changes of low-density-lipoprotein cholesterol or CRP, after sex, age, and statin type were adjusted. We also revealed that RhoA and transforming growth factor-β signaling pathways might be regulated by the four miRNAs. Given our findings, miRNAs might be involved in statin-induced inflammation modulation in PBMCs, providing likelihood to assess and reduce inflammation in patients with atherosclerotic cardiovascular diseases.

Norepinephrine Inhibits Energy Metabolism of Human Peripheral Blood Mononuclear Cells via Adrenergic Receptors

2001 ◽  
Vol 21 (5) ◽  
pp. 627-635 ◽  
Author(s):  
Jan D. Lünemann ◽  
Frank Buttgereit ◽  
Robert Tripmacher ◽  
Christoph G. O. Baerwald ◽  
Gerd-Rüdiger Burmester ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Peripheral Blood Mononuclear Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Adrenergic Receptors ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Immune Effector ◽  
Blood Mononuclear Cells

Previous studies demonstrated that the adaptive response to stressors and inflammatory signals involves the activation of the automotic nervous system. Catecholamines have been shown to modulate the activity of various immune effector cells directly via membrane adrenergic receptors. Here, we investigated immediate effects of norepinephrine on energy metabolism of immune cells. Norepinephrine inhibits oxygen consumption of human peripheral blood mononuclear cells at concentrations that are relevant to its physiological range. The ?-adrenoreceptor antagonist propranolol, but not the ?-adrenoreceptor antagonist phentolamine reversed the norepinephrine induced inhibition in quiescent cells. Conversely, phentolamine but not propranolol is capable of blocking norepinephrine mediated effects in mitogen activated human peripheral blood mononuclear cells. Our data indicate that the sensitization of ?- and ?-adrenoreceptors on immune cells is differentially regulated, and that these processes depend on the activation state of these cells. These findings have important implications for the understanding of stress-induced suppression of immune function and may contribute to the elucidation of the pathogenesis of immunologically mediated diseases.

scholarly journals Function of ex vivo stimulated Natural killer T cells from patients with chronic HIV-1 infection

2019 ◽  
Author(s):  
Prakash Thapa ◽  
Pramod Nehete ◽  
Hong He ◽  
Bharti Nehete ◽  
Stephanie J. Buchl ◽  
...  
Keyword(s):  
Natural Killer ◽  
Peripheral Blood Mononuclear Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Nkt Cells ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Hiv 1

AbstractNatural killer T (NKT) cells are innate immune cells that are responsible for the first line of antiviral defense, through crosstalk with downstream antigen-presenting cells, natural killer cells, and adaptive immune cells. Previous studies have indicated that NKT cell function is severely impaired in patients with chronic HIV-1 infection. It was reported that alpha-galactosylceramide, a potent agonist antigen for NKT cells, failed to trigger the expansion of NKT cells, or the production of anti-viral cytokines by NKT cells from HIV-1 infected patients in an in vitro assay, in which peripheral blood mononuclear cells (PBMCs) were cultured in the presence of alpha-galactosylceramide. In this study, we stimulated banked peripheral blood mononuclear cells from HIV-1-infected patients with dendritic cells (DC) generated ex vivo and loaded with alpha-galactosylceramide. The results showed that NKT cells were expanded in HIV infected subjects except in patients with advanced AIDS. Expanded NKT cells were capable of producing antiviral cytokines. Our results indicate that NKT cells in HIV infected individuals are potential targets for therapeutic intervention.

Identification Of Specific Hematopoietic Populations Present In Peripheral Blood Mononuclear Cells That Increase Erythroid Output Directly Or Through Feeder/Stromal Cell-Like Properties

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3414-3414
Author(s):  
Esther Heideveld ◽  
Valentina Tirelli ◽  
Francesca Masiello ◽  
Fatemehsadat Esteghamat ◽  
Nurcan Yagci ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Fold Increase ◽  
Cell Contact ◽  
Peripheral Blood Mononuclear ◽  
Effector Cells ◽  
Cd34 Cells ◽  
Blood Mononuclear Cells

Abstract Hematopoietic development occurs in defined niches that ensure specific interactions and cross-talk with the surrounding stromal cells and different hematopoietic cells themselves. For instance, erythropoiesis occurs on the macrophage island within the bone marrow and the central macrophage is believed to regulate pro-erythroblast differentiation, the final stages of enucleation and reticulocyte maturation. We have observed that the expansion of erythroblasts from total peripheral blood mononuclear cells is increased compared to CD34+ Hematopoietic Stem/Progenitor Cells (HS(P)C) isolated from the same amount of blood [van den Akker, Haematologica, 2010]. This suggests i) the presence of CD34-cells that contribute to erythropoiesis and/or ii) that cell-cell contact or specific secreted growth factors by “helper” cells in these cultures can regulate hematopoiesis/erythropoiesis to increase erythroblast yield. Identifying the specific population(s) underlying the increased erythroid yield and understanding their way of action and regulatory mechanism during HSC differentiation and erythropoiesis is not only important to improve erythroblast culture conditions but may also provide clues to the function of hematopoietic effector cells in the various HS(P)C/erythroblast niches. Using specific lineage depletion (among which CD3 and CD14) we have identified and quantified various human erythroid and non-erythroid CD34+ and CD34- populations on the basis of CD36 co-expression in peripheral blood mononuclear cells (PBMC). Erythroid outgrowth from these CD34- populations and CD34+ populations and their contribution to the total erythroid yield from PBMC was assessed. Interestingly, total erythroid yield from the individual sorted populations did not reach the erythroid yield obtained from total PBMC. We hypothesized that support/feeder cells present in total PBMC are positively influencing in vitro erythropoiesis. In agreement with this, PBMC immuno-depletion of specific hematopoietic cell types identified CD14 cells (monocyte/macrophages) and to a lesser extend CD3 cells (lymphocytes) to be also partly responsible for the increased erythroblast yield. Compared to HS(P)C alone, co-culture of CD14 cells and HS(P)C isolated from PBMC resulted in a 5-10 times increase in CD71high/CD235med erythroblasts. Conditioned medium of CD14 cells as well as transwell experiments reconstituted the effect of the HS(P)C-CD14 co-cultures to 70%-80%, indicating that cell-cell contact plays a minor role. CD14 cells could elicit their effect at different stages during HSPC/HSC differentiation to erythroblasts. Co-culture of CD14 cells with pro-erythroblasts did not increase the cellular yield or proliferation rate. In contrast, two days of CD14 co-culture with CD34+ cells results in a 5 fold increase of total colony forming units without altering the colony lineage dynamics. In agreement with this a 5 fold increase in CD34+ cells was observed. These results indicate that CD14 cells elicit their effect on early hematopoietic progenitors but not on the erythroblast population. The results predict that depletion of CD14+ cells from PBMC should result in a decrease in the total number of CD34+cells. Indeed, we observed a 2 fold decrease of specifically HS(P)Cs and MEPs after two days of culture in PBMCs depleted for CD14 cells. Taken together our data i) identify previously unrecognized erythroid and non erythroid CD34- and CD34+ populations in peripheral blood that contribute to erythroid yield from total PBMC and ii) indicate modulation of HS(P)C outgrowth by specific hematopioietic effector cells present in peripheral blood that can also be found near specific hematopoietic niches in the bone marrow. The involvement of CD3 and CD14 immune cells suggests that HS(P)C and erythropoiesis may be modulated by immune-responses. Disclosures: No relevant conflicts of interest to declare.

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