Immune Enhancing Activity of β-(1,3)-Glucan Isolated from Genus Agrobacterium in Bone-Marrow Derived Macrophages and Mice Splenocytes

2016 ◽  
Vol 44 (05) ◽  
pp. 1009-1026 ◽  
Author(s):  
Eui-Baek Byun ◽  
Beom-Su Jang ◽  
Eui-Hong Byun ◽  
Nak-Yun Sung
Keyword(s):  
Immune Response ◽  
Macrophage Activation ◽  
Transmembrane Protein ◽  
Signaling Mechanism ◽  
Th2 Cytokine ◽  
Mitogen Activated Protein ◽  
Th1 Cytokine ◽  
Th1 Polarization ◽  
Necrosis Factor ◽  
Immunomodulation Effect

An effective method for activating macrophages and deriving a Th1 immune response could be used to improve the defenses of hosts. In this study, we investigated the immunomodulation effect and the related signaling mechanism of [Formula: see text]-(1,3)-glucan, isolated from the Agrobacterium species. Here, we found that [Formula: see text]-(1,3)-glucan predominantly induced the tumor necrosis factor (TNF)-[Formula: see text], interleukin (IL)-1[Formula: see text], IL-6, IL-12p70, and nitric oxide, which was dependent on mitogen-activated protein kinases (MAPK) and nuclear factor (NF)-[Formula: see text]B signaling. Additionally, [Formula: see text]-(1,3)-glucan treatment significantly up-regulated the expression of the co-stimulatory molecules CD80 and CD86, and also significantly increased the expression of iNOS and Dectin-1, which is a transmembrane protein that binds [Formula: see text]-glucan and associates with macrophage activation. Importantly, the splenic T cells co-cultured with [Formula: see text]-(1,3)-glucan-treated macrophages produced the a Th1 cytokine profile that includes high levels of IFN-[Formula: see text], but not IL-4 (Th2 cytokine), indicating that [Formula: see text]-(1,3)-glucan contributes to Th1 polarization of the immune response. Taken together, our results suggest that [Formula: see text]-(1,3)-glucan isolated from Agrobacterium species can induce macrophage activation through the MAPK and NF-[Formula: see text]B signaling pathway, as well as Th1 polarization.

scholarly journals Th1 Polarization of Cytokine and Cytokine Receptor Polymorphisms Affect the Susceptibility and Severity of ITP

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2245-2245
Author(s):  
Noriyuki Takahashi ◽  
Takayuki Saitoh ◽  
Nanami Gotoh ◽  
Kei Kimura ◽  
Yuko Kuroda ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Steroid Treatment ◽  
Cytokine Receptor ◽  
Function Type ◽  
Chronic Itp ◽  
Th2 Cytokine ◽  
Th1 Cytokine ◽  
Ifn Γ ◽  
Th1 Polarization ◽  
Low Expression

Abstract Introduction: Immune thrombocytopenia (ITP) is an acquired autoimmune disorder characterized by the production of platelet antibodies, resulting in the destruction of platelets and inhibition of their production. Many cytokine profile study have revealed a clear T helper type1 (Th1) cytokine polarization in chronic ITP patients, using quantitative RT-PCR and flow cytometry method. However, it remains unclear whether genetic factors of Th1/Th2 cytokine and cytokine receptor affect chronic ITP. We investigated the impact of IFN-γ+874T/A, IFN-γ receptor (R) -611G/A, IL-4 -590C/T, and IL-4 receptor (R) a Q576R polymorphisms on the susceptibility and clinical feature of chronic ITP and Th1/Th2 ratio in peripheral blood of ITP patients, Patients and methods: Genotyping was determined by PCR based technique and direct sequencing. The diagnosis and response criteria of the ITP were defined according to International Working Group criteria. We evaluated Th1/Th2 ratio in peripheral blood of 15 normal donors and 25 ITP patients by intracellular flow cytometry. Intracellular IL-4 (Th2 cytokine) and IFN-γ (Th1 cytokine) production was assessed in CD4+ T lymphocytes activated by phorbol 12-myristate 13-acetate and ionomycin by flow cytometry. This study was approved by the IRB of our hospital. Results: The platelet count ranged from 1´109/L to 98´109/L with a mean count of 32´109/L at the initial diagnosis. Eighty-three patients (56.1%) had bleeding tendency and 24 patients (16.2%) had severe thrombocytopenia (< 10 ´109/L). Steroid treatment was given to 86 patients (58.1%), and eradication of Helicobacter pylori was performed in 38 patients (25.7%), while splenectomy was performed in only 18 patients (12.2%). As compared to control group, chronic ITP patients had significantly higher frequency of the IL-4R576 non-QQ (low function type) than QQ (high function type) (29.7% vs 15.2%, P<0.05). ITP patients with IL-4-590 CC genotype (low expression type) showed lower platelet counts than those with IL-4-590 non-CC genotype (high expression type) (21±17 X109/mL vs 33±27 X109/mL, p<0.05). ITP patients with IFN-γ+874 non-AA genotype (high expression type) showed lower response rate to steroid treatment than those with IFN-γ+874 AA genotype (low expression type) (76.9% vs 97.5%, p<0.05). We examined the association between Th1/Th2 polymorphisms and Th1/Th2 ratio in both normal donors and ITP patients. Th1/Th2 ratio was not significantly different among IFN-γ+874T/A, IFN-γR-611G/A, IL-4-590C/T, and IL-4Ra Q576R polymorphisms in normal donors. In contrast, ITP patients with IL-4Ra576 non-QQ genotype (low function type) had higher tendency of Th1/Th2 ratio compared to IL-4Ra576 QQ genotype (high function type) (111.2±216.1 vs. 20.8±21.6, p = 0.12). Conclusion: These findings suggested that Th1 polarization of Th1/Th2 cytokine and cytokine receptor polymorphisms affect the susceptibility and severity of chronic ITP. Especially, IL-4Ra576 QQ genotype may be closely associated with the risk of ITP and Th1 polarization. Disclosures No relevant conflicts of interest to declare.

scholarly journals Combination of vegetable soup and glucan demonstrates synergistic effects on macrophage-mediated immune responses

2021 ◽  
Vol 30 (4) ◽  
pp. 583-588
Author(s):  
Ha-Nul Lee ◽  
Joo-Hee Choi ◽  
Ji-Yeon Park ◽  
Jae-Hun Ahn ◽  
Da Eun Jang ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Synergistic Effects ◽  
Folk Medicine ◽  
Mitogen Activated Protein Kinase ◽  
Vegetable Soup ◽  
Mitogen Activated Protein ◽  
Factor Α ◽  
Further Development ◽  
Necrosis Factor

AbstractVegetable soup (VS), a plant-based functional food, has been used as a traditional folk medicine and is attracting attention for its ability to enhance the immune response. β-Glucan, a well-established and effective immunomodulator, has synergistic effects when used in combination with some bioactive compounds. In the present study, we aimed to evaluate the synergistic immunomodulatory effects of the combination of VS and β-glucan on macrophage-mediated immune responses. β-Glucan was demonstrated to synergistically enhance the VS-stimulated immune response, including the production of interleukin-6, tumor necrosis factor-α, and nitric oxide, mainly through the mitogen-activated protein kinase pathway in macrophages. In addition, this combination has the potential for further development in functional foods with immune-enhancing activity.

scholarly journals PKCϵ is involved in JNK activation that mediates LPS-induced TNF-α, which induces apoptosis in macrophages

2003 ◽  
Vol 285 (5) ◽  
pp. C1235-C1245 ◽  
Author(s):  
Mònica Comalada ◽  
Jordi Xaus ◽  
Annabel F. Valledor ◽  
Carlos López-López ◽  
Daniel J. Pennington ◽  
...  
Keyword(s):  
Cell Model ◽  
Primary Cultures ◽  
Signaling Mechanism ◽  
Major Function ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Jnk Activation ◽  
Necrosis Factor

Lipopolysaccharide (LPS) is a powerful stimulator of macrophages and induces apoptosis in these cells. Using primary cultures of bone marrow-derived macrophages, we found that the autocrine production of tumor necrosis factor-α (TNF-α) has a major function in LPS-induced apoptosis. LPS activates PKC and regulates the different mitogen-activated protein kinases (MAPK). We aimed to determine its involvement either in the secretion of TNF-α or in the induction of apoptosis. Using specific inhibitors and mice with the gene for PKCϵ disrupted, we found that LPS-induced TNF-α-dependent apoptosis is mostly mediated by PKCϵ, which is not directly involved in the signaling mechanism of apoptosis but rather in the process of TNF-α secretion. In our cell model, all three MAPKs were involved in the regulation of TNF-α secretion, but at different levels. JNK mainly regulates TNF-α transcription and apoptosis, whereas ERK and p38 contribute to the regulation of TNF-α production, probably through posttranscriptional mechanisms. Only JNK activity is mediated by PKCϵ in response to LPS and so plays a major role in TNF-α secretion and LPS-induced apoptosis. We demonstrated in macrophages that LPS involving PKCϵ regulates JNK activity and produces TNF-α, which induces apoptosis.

Hyperferritinaemia: An Iron Sword of Autoimmunity

2019 ◽  
Vol 25 (27) ◽  
pp. 2909-2918 ◽  
Author(s):  
Joanna Giemza-Stokłosa ◽  
Md. Asiful Islam ◽  
Przemysław J. Kotyla
Keyword(s):  
Immune Response ◽  
Macrophage Activation ◽  
Inflammatory Diseases ◽  
Acute Phase Reactant ◽  
Catastrophic Antiphospholipid Syndrome ◽  
Inflammatory Conditions ◽  
Phase Reactant ◽  
Signalling Molecule ◽  
Cytokine Synthesis

Background:: Ferritin is a molecule that plays many roles being the storage for iron, signalling molecule, and modulator of the immune response. Methods:: Different electronic databases were searched in a non-systematic way to find out the literature of interest. Results:: The level of ferritin rises in many inflammatory conditions including autoimmune disorders. However, in four inflammatory diseases (i.e., adult-onset Still’s diseases, macrophage activation syndrome, catastrophic antiphospholipid syndrome, and sepsis), high levels of ferritin are observed suggesting it as a remarkable biomarker and pathological involvement in these diseases. Acting as an acute phase reactant, ferritin is also involved in the cytokine-associated modulator of the immune response as well as a regulator of cytokine synthesis and release which are responsible for the inflammatory storm. Conclusion:: This review article presents updated information on the role of ferritin in inflammatory and autoimmune diseases with an emphasis on hyperferritinaemic syndrome.

scholarly journals Death of unknown cause? Post-mortem diagnosis of fulminant course of an EBV-associated secondary hemophagocytic lymphohistiocytosis

2021 ◽  
Author(s):  
Josia Fauser ◽  
Stefan Köck ◽  
Eberhard Gunsilius ◽  
Andreas Chott ◽  
Andreas Peer ◽  
...  
Keyword(s):  
Immune Response ◽  
Case Report ◽  
Macrophage Activation ◽  
Post Mortem ◽  
Life Threatening ◽  
Appropriate Therapy ◽  
Diagnostic Work ◽  
Work Up ◽  
Diagnostic Work Up ◽  
Secondary Hemophagocytic Lymphohistiocytosis

SummaryHLH is a life-threatening disease, which is characterized by a dysregulated immune response with uncontrolled T cell and macrophage activation. The often fulminant course of the disease needs a fast diagnostic work-up to initiate as soon as possible the appropriate therapy. We present herein the case of a 71-year-old patient with rapidly progressive hyperinflammatory syndrome, which post mortem resulted in the diagnosis of EBV-associated HLH. With this case report, we intend to highlight the relevance of the HScore in the diagnosis of HLH, to create a greater awareness for EBV as a trigger of HLH, and to demonstrate the importance of treating EBV-associated HLH as early as possible.

scholarly journals The Role of Th17 Response in COVID-19

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1550
Author(s):  
Diana Martonik ◽  
Anna Parfieniuk-Kowerda ◽  
Magdalena Rogalska ◽  
Robert Flisiak
Keyword(s):  
Immune Response ◽  
Treg Cells ◽  
The Body ◽  
System Response ◽  
Th17 Response ◽  
Monocyte Chemoattractant Protein 1 ◽  
Acute Infectious Disease ◽  
Cytokine Cascade ◽  
Necrosis Factor

COVID-19 is an acute infectious disease of the respiratory system caused by infection with the SARS-CoV-2 virus (Severe Acute Respiratory Syndrome Coronavirus 2). Transmission of SARS-CoV-2 infections occurs through droplets and contaminated objects. A rapid and well-coordinated immune system response is the first line of defense in a viral infection. However, a disturbed and over-activated immune response may be counterproductive, causing damage to the body. Severely ill patients hospitalised with COVID-19 exhibit increased levels of many cytokines, including Interleukin (IL)-1β, IL-2, IL-6, IL-7, IL-8, IL-10, IL-17, granulocyte colony stimulating factor (G-CSF), monocyte chemoattractant protein 1 (MCP-1) and tumor necrosis factor (TNF). Increasing evidence suggests that Th17 cells play an important role in the pathogenesis of COVID-19, not only by activating cytokine cascade but also by inducing Th2 responses, inhibiting Th1 differentiation and suppressing Treg cells. This review focuses on a Th17 pathway in the course of the immune response in COVID-19, and explores plausible targets for therapeutic intervention.

scholarly journals Macrophage Activation and Cytokine Release Syndrome in COVID-19: Current Updates and Analysis of Repurposed and Investigational Anti-Cytokine Drugs

Drug Research ◽  
2021 ◽  
Author(s):  
Ashif Iqubal ◽  
Farazul Hoda ◽  
Abul Kalam Najmi ◽  
Syed Ehtaishamul Haque
Keyword(s):  
Immune Response ◽  
Clinical Trials ◽  
Macrophage Activation ◽  
Fatality Rate ◽  
Cytokine Storm ◽  
Cytokine Release ◽  
Cytokine Release Syndrome ◽  
Disease Condition ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

AbstractCoronavirus disease (COVID-19) emerged from Wuhan, has now become pandemic and the mortality rate is growing exponentially. Clinical complication and fatality rate is much higher for patients having co-morbid issues. Compromised immune response and hyper inflammation is hall mark of pathogenesis and major cause of mortality. Cytokine release syndrome (CRS) or cytokine storm is a term used to affiliate the situation of hyper inflammation and therefore use of anti-cytokine and anti-inflammatory drugs is used to take care of this situation. Looking into the clinical benefit of these anti-inflammatory drugs, many of them enter into clinical trials. However, understanding the immunopathology of COVID-19 is important otherwise, indiscriminate use of these drugs could be fetal as there exists a very fine line of difference between viral clearing cytokines and inflammatory cytokines. If any drug suppresses the viral clearing cytokines, it will worsen the situation and hence, the use of these drugs must be based on the clinical condition, viral load, co-existing disease condition and severity of the infection.

scholarly journals Chrysin Inhibits TNFα-Induced TSLP Expression through Downregulation of EGR1 Expression in Keratinocytes

2021 ◽  
Vol 22 (9) ◽  
pp. 4350
Author(s):  
Hyunjin Yeo ◽  
Younghan Lee ◽  
Sungshin Ahn ◽  
Euitaek Jung ◽  
Yoongho Lim ◽  
...  
Keyword(s):  
Clinical Symptoms ◽  
Skin Lesions ◽  
Therapeutic Agents ◽  
Mitogen Activated Protein Kinase ◽  
Necrosis Factor Alpha ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Signaling Axis ◽  
Factor Alpha ◽  
Necrosis Factor

Thymic stromal lymphopoietin (TSLP) is an epithelial cell-derived cytokine that acts as a critical mediator in the pathogenesis of atopic dermatitis (AD). Various therapeutic agents that prevent TSLP function can efficiently relieve the clinical symptoms of AD. However, the downregulation of TSLP expression by therapeutic agents remains poorly understood. In this study, we investigated the mode of action of chrysin in TSLP suppression in an AD-like inflammatory environment. We observed that the transcription factor early growth response (EGR1) contributed to the tumor necrosis factor alpha (TNFα)-induced transcription of TSLP. Chrysin attenuated TNFα-induced TSLP expression by downregulating EGR1 expression in HaCaT keratinocytes. We also showed that the oral administration of chrysin improved AD-like skin lesions in the ear and neck of BALB/c mice challenged with 2,4-dinitrochlorobenzene. We also showed that chrysin suppressed the expression of EGR1 and TSLP by inhibiting the extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) 1/2 mitogen-activated protein kinase pathways. Collectively, the findings of this study suggest that chrysin improves AD-like skin lesions, at least in part, through the downregulation of the ERK1/2 or JNK1/2-EGR1-TSLP signaling axis in keratinocytes.

scholarly journals Effect of Novel Marine Nutraceuticals on IL-1α-Mediated TNF-αRelease from UVB-Irradiated Human Melanocyte-Derived Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Visalini Muthusamy ◽  
Lynn D. Hodges ◽  
Theodore A. Macrides ◽  
Glen M. Boyle ◽  
Terrence J. Piva
Keyword(s):  
Antioxidant Properties ◽  
Mitogen Activated Protein Kinase ◽  
Uvb Radiation ◽  
Reactive Oxygen Species Formation ◽  
Mapk Signalling Pathway ◽  
Species Formation ◽  
Human Melanocyte ◽  
Mapk Signalling ◽  
Mitogen Activated Protein ◽  
Necrosis Factor

UV-induced inflammation and reactive oxygen species formation are involved in the development of melanoma. Natural products like 5β-scymnol and CO2-supercritical fluid extract (CO2-SFE) of mussel oil contain anti-inflammatory and antioxidant properties that may aid in reducing the deleterious effects of UV radiation. Therefore, their effect on the release of the proinflammatory cytokine, tumour necrosis factor-α(TNF-α), from UVB-irradiated human melanocytic cells was examined. Human epidermal melanocytes (HEM) and MM96L melanoma cells were exposed to UVB radiation and IL-1α. Cell viability and TNF-αlevels were determined 24 hours after-irradiation while p38 mitogen-activated protein kinase (MAPK) activation was observed at 15 min after-irradiation. Whenα-tocopherol, CO2-SFE mussel oil, and 5β-scymnol were added to the UVB-irradiated HEM cells treated with IL-1α, TNF-αlevels fell by 53%, 65%, and 76%, respectively, while no inhibition was evident in MM96L cells. This effect was not due to inhibition of the intracellular p38 MAPK signalling pathway. These compounds may be useful in preventing inflammation-induced damage to normal melanocytes.

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