scholarly journals Profound inhibition of CD73-dependent formation of anti-inflammatory adenosine in B cells of SLE patients

EBioMedicine ◽  
2021 ◽  
Vol 73 ◽  
pp. 103616
Author(s):  
Julia Hesse ◽  
Magdalena Siekierka-Harreis ◽  
Bodo Steckel ◽  
Christina Alter ◽  
Merle Schallehn ◽  
...  
Keyword(s):  
B Cells ◽  
Anti Inflammatory

scholarly journals Anti-Inflammatory and Chondroprotective Effects of Vanillic Acid and Epimedin C in Human Osteoarthritic Chondrocytes

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 932
Author(s):  
Reihane Ziadlou ◽  
Andrea Barbero ◽  
Ivan Martin ◽  
Xinluan Wang ◽  
Ling Qin ◽  
...  
Keyword(s):  
B Cells ◽  
Vanillic Acid ◽  
Ex Vivo ◽  
Cartilage Regeneration ◽  
Nuclear Factor ◽  
Treatment Groups ◽  
Extracellular Matrix Components ◽  
Gene Enhancer ◽  
Anti Inflammatory ◽  
Factor Α

In osteoarthritis (OA), inhibition of excessively expressed pro-inflammatory cytokines in the OA joint and increasing the anabolism for cartilage regeneration are necessary. In this ex-vivo study, we used an inflammatory model of human OA chondrocytes microtissues, consisting of treatment with cytokines (interleukin 1β (IL-1β)/tumor necrosis factor α (TNF-α)) with or without supplementation of six herbal compounds with previously identified chondroprotective effect. The compounds were assessed for their capacity to modulate the key catabolic and anabolic factors using several molecular analyses. We selectively investigated the mechanism of action of the two most potent compounds Vanillic acid (VA) and Epimedin C (Epi C). After identification of the anti-inflammatory and anabolic properties of VA and Epi C, the Ingenuity Pathway Analysis showed that in both treatment groups, osteoarthritic signaling pathways were inhibited. In the treatment group with VA, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling was inhibited by attenuation of the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα) phosphorylation. Epi C showed a significant anabolic effect by increasing the expression of collagenous and non-collagenous matrix proteins. In conclusion, VA, through inhibition of phosphorylation in NF-κB signaling pathway and Epi C, by increasing the expression of extracellular matrix components, showed significant anti-inflammatory and anabolic properties and might be potentially used in combination to treat or prevent joint OA.

scholarly journals Anti-Inflammatory Activities of Captopril and Diuretics on Macrophage Activity in Mouse Humoral Immune Response

2021 ◽  
Vol 22 (21) ◽  
pp. 11374
Author(s):  
Paweł Bryniarski ◽  
Katarzyna Nazimek ◽  
Janusz Marcinkiewicz
Keyword(s):  
Immune Response ◽  
B Cells ◽  
Humoral Immune Response ◽  
Humoral Response ◽  
Peritoneal Macrophages ◽  
Surface Markers ◽  
Immunomodulatory Effects ◽  
Humoral Immune ◽  
Macrophage Activity ◽  
Anti Inflammatory

Hypertension is accompanied by the over-activation of macrophages. Diuretics administered alone or in combination with hypotensive drugs may have immunomodulatory effects. Thus, the influence of tested drugs on mouse macrophage-mediated humoral immunity was investigated. Mice were treated intraperitoneally with captopril (5 mg/kg) with or without hydrochlorothiazide (10 mg/kg) or furosemide (5 mg/kg) by 8 days. Mineral oil-induced peritoneal macrophages were harvested to assess the generation of cytokines in ELISA, and the expression of surface markers was analyzed cytometrically. Macrophages were also pulsed with sheep red blood cells (SRBC) and transferred to naive mice for evaluation of their ability to induce a humoral immune response. Tested drugs increase the expression of surface markers important for the antigen phagocytosis and presentation. SRBC-pulsed macrophages from mice treated with captopril combined with diuretics increased the secretion of antigen-specific antibodies by recipient B cells, while macrophages of mice treated with hydrochlorothiazide or furosemide with captopril increased the number of antigen-specific B cells. Tested drugs alter the macrophage secretory profile in favor of anti-inflammatory cytokines. Our results showed that diuretics with or without captopril modulate the humoral response by affecting the function of macrophages, which has significant translational potential in assessing the safety of antihypertensive therapy.

Imbalance in pro-inflammatory and anti-inflammatory cytokines milieu in B cells of children with autism

2022 ◽  
Vol 141 ◽  
pp. 297-304
Author(s):  
Ahmed Nadeem ◽  
Sheikh F. Ahmad ◽  
Naif O. Al-Harbi ◽  
Laila Y. AL-Ayadhi ◽  
Wedad Sarawi ◽  
...  
Keyword(s):  
B Cells ◽  
Inflammatory Cytokines ◽  
Children With Autism ◽  
Anti Inflammatory

scholarly journals Mesenchymal Stem Cell Derived Biocompatible Membrane Vesicles Demonstrate Immunomodulatory Activity Inhibiting Activation and Proliferation of Human Mononuclear Cells

Pharmaceutics ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 577
Author(s):  
Marina Gomzikova ◽  
Sevindzh Kletukhina ◽  
Sirina Kurbangaleeva ◽  
Olga Neustroeva ◽  
Olga Vasileva ◽  
...  
Keyword(s):  
Immune Response ◽  
Stem Cell ◽  
B Cells ◽  
T Lymphocytes ◽  
Mesenchymal Stem Cell ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Membrane Vesicles ◽  
Immunomodulatory Activity ◽  
Anti Inflammatory

Immune-mediated diseases are characterized by abnormal activity of the immune system. The cytochalasin B-induced membrane vesicles (CIMVs) are innovative therapeutic instruments. However, the immunomodulating activity of human mesenchymal stem cell (MSC)-derived CIMVs (CIMVs-MSCs) remains unknown. Therefore, we sought to investigate the immunological properties of CIMVs-MSCs and evaluate their effect on human peripheral blood mononuclear cells (PBMCs). We found that CIMVs-MSCs are primarily uptaken by monocytes and B-cells. Additionally, we demonstrated that CIMVs-MSCs inhibit phytohemagglutinin (PHA)-induced proliferation of PBMCs, with more pronounced effect on T-lymphocytes expansion as compared to that of B-cells. In addition, activation of T-helpers (CD4+CD25+), B-cells (CD19+CD25+), and T-cytotoxic lymphocytes (CD8+CD25+) was also significantly suppressed by CIMVs-MSCs. Additionally, CIMVs-MSCs decreased secretion of epidermal growth factor (EGF) and pro-inflammatory Fractalkine in a population of PBMCs, while the releases of FGF-2, G-CSF, anti-inflammatory GM-CSF, MCP-3, anti-inflammatory MDC, anti-inflammatory IL-12p70, pro-inflammatory IL-1b, and MCP-1 were increased. We analyzed the effect of CIMVs-MSCs on an isolated population of CD4+ and CD8+ T-lymphocytes and demonstrated their different immune response and cytokine secretion. Finally, we observed that no xenogeneic nor allogeneic transplantation of CIMVs induced an immune response in mice. Our data suggest that CIMVs-MSCs have immunosuppressive properties, are potential agents for immunomodulating treatment, and are worthy of further investigation.

Mesenchymal stem cells induced anti-inflammatory features in B cells from breast tumor draining lymph nodes

2018 ◽  
Vol 42 (12) ◽  
pp. 1658-1669 ◽  
Author(s):  
Fereshteh Mehdipour ◽  
Mahboobeh Razmkhah ◽  
Somayeh Rezaeifard ◽  
Mandana Bagheri ◽  
Abdol-Rasoul Talei ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
B Cells ◽  
Lymph Nodes ◽  
Breast Tumor ◽  
Anti Inflammatory ◽  
Draining Lymph Nodes

scholarly journals Complex human adenoid tissue-based ex vivo culture systems reveal anti-inflammatory drug effects on germinal center T and B cells

EBioMedicine ◽  
2020 ◽  
Vol 53 ◽  
pp. 102684 ◽  
Author(s):  
Angelika Schmidt ◽  
Johanna E. Huber ◽  
Özen Sercan Alp ◽  
Robert Gürkov ◽  
Christoph A. Reichel ◽  
...  
Keyword(s):  
B Cells ◽  
Germinal Center ◽  
Ex Vivo ◽  
Drug Effects ◽  
T And B Cells ◽  
Inflammatory Drug ◽  
Culture Systems ◽  
Adenoid Tissue ◽  
Anti Inflammatory ◽  
Ex Vivo Culture

scholarly journals B Cells in Neuroinflammation: New Perspectives and Mechanistic Insights

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1605
Author(s):  
Julie J. Ahn ◽  
Mohammad Abu-Rub ◽  
Robert H. Miller
Keyword(s):  
B Cells ◽  
B Cell ◽  
Neurological Disorders ◽  
Inflammatory Diseases ◽  
Neurological Diseases ◽  
Adaptive Immune System ◽  
Inflammatory Processes ◽  
Anti Inflammatory ◽  
Neurological Processes

In recent years, the role of B cells in neurological disorders has substantially expanded our perspectives on mechanisms of neuroinflammation. The success of B cell-depleting therapies in patients with CNS diseases such as neuromyelitis optica and multiple sclerosis has highlighted the importance of neuroimmune crosstalk in inflammatory processes. While B cells are essential for the adaptive immune system and antibody production, they are also major contributors of pro- and anti-inflammatory cytokine responses in a number of inflammatory diseases. B cells can contribute to neurological diseases through peripheral immune mechanisms, including production of cytokines and antibodies, or through CNS mechanisms following compartmentalization. Emerging evidence suggests that aberrant pro- or anti-inflammatory B cell populations contribute to neurological processes, including glial activation, which has been implicated in the pathogenesis of several neurodegenerative diseases. In this review, we summarize recent findings on B cell involvement in neuroinflammatory diseases and discuss evidence to support pathogenic immunomodulatory functions of B cells in neurological disorders, highlighting the importance of B cell-directed therapies.

scholarly journals Dopaminergic stimulation leads B-cell infiltration into the central nervous system upon autoimmunity

2020 ◽  
Author(s):  
Carolina Prado ◽  
Francisco Osorio-Barrios ◽  
Alexandra Espinoza ◽  
Juan J Saez ◽  
María I Yuseff ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
T Cell ◽  
B Cells ◽  
Animal Models ◽  
B Cell ◽  
T Cell Response ◽  
Autoimmune Response ◽  
Cns Autoimmunity ◽  
Anti Inflammatory

Abstract Background: Recent evidence has shown dopamine as a major regulator of inflammation. Accordingly, dopaminergic regulation of adaptive and innate immune cells plays an important role in the physiopathology of inflammatory disorders. Multiple sclerosis (MS) is an inflammatory disease involving a CD4+ T-cell-driven autoimmune response to central nervous system (CNS) derived antigens. Evidence from animal models has suggested that B-cells play a fundamental role as antigen-presenting cells (APC) re-stimulating CD4+ T-cells in the CNS as well as regulating T-cell response by mean of inflammatory or anti-inflammatory cytokines. Here we addressed the role of the dopamine receptor D3 (DRD3), which display the highest affinity for dopamine, in B-cells in animal models of MS.Methods: Mice harbouring Drd3-deficient or Drd3-suficient B-cells were generated by bone marrow transplantation into recipient mice devoid of B-cells. In these mice we compare the development of experimental autoimmune encephalomyelitis (EAE) induced by immunization with a myelin oligodendrocyte glycoprotein (MOG)-derived peptide (pMOG), a model that leads to CNS-autoimmunity irrespective of the APC function of B-cells, or by immunization with full-length human MOG protein (huMOG), a model in which antigen-specific activated B-cells display a fundamental APCs function in the CNS. Results: Our data shows that, by promoting the expression of the chemokine receptor CXCR3 in autoreactive B-cells, DRD3-stimulation favours the CNS-tropism in a subset of B-cells that act as APC in the CNS, which is fundamental for disease development. Furthermore, we found that DRD3- stimulation induced the expression of the CNS-homing molecule CD49d in a B-cell subset with anti-inflammatory features, thus attenuating EAE manifestation in a CNS-autoimmunity model independent of the APC function of B-cells.Conclusion: Our findings demonstrate that DRD3-stimulation in B-cells exerts a dual role in CNS-autoimmunity, favouring CNS-tropism of pro-inflammatory B-cells with APC function, and also promoting CNS-homing of B-cells with anti-inflammatory features. Thus, these results show DRD3-stimulation in B-cells as a key regulator of CNS-autoimmunity.

Sign in / Sign up

Export Citation Format

Share Document