scholarly journals Glutathione Supplementation as an Adjunctive Therapy in COVID-19

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 914
Author(s):  
Vika Guloyan ◽  
Buzand Oganesian ◽  
Nicole Baghdasaryan ◽  
Christopher Yeh ◽  
Manpreet Singh ◽  
...  
Keyword(s):  
Disease Process ◽  
Current Treatment ◽  
Treatment Modalities ◽  
Adjunctive Treatment ◽  
Interferon Α ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Factor Α ◽  
Necrosis Factor

Morbidity and mortality of coronavirus disease 2019 (COVID-19) are due in large part to severe cytokine storm and hypercoagulable state brought on by dysregulated host-inflammatory immune response, ultimately leading to multi-organ failure. Exacerbated oxidative stress caused by increased levels of interleukin (IL)-6 and tumor necrosis factor α (TNF-α) along with decreased levels of interferon α and interferon β (IFN-α, IFN-β) are mainly believed to drive the disease process. Based on the evidence attesting to the ability of glutathione (GSH) to inhibit viral replication and decrease levels of IL-6 in human immunodeficiency virus (HIV) and tuberculosis (TB) patients, as well as beneficial effects of GSH on other pulmonary diseases processes, we believe the use of liposomal GSH could be beneficial in COVID-19 patients. This review discusses the epidemiology, transmission, and clinical presentation of COVID-19 with a focus on its pathogenesis and the possible use of liposomal GSH as an adjunctive treatment to the current treatment modalities in COVID-19 patients.

scholarly journals Antibody-Mediated Porcine Reproductive and Respiratory Syndrome Virus Infection Downregulates the Production of Interferon-α and Tumor Necrosis Factor-α in Porcine Alveolar Macrophages via Fc Gamma Receptor I and III

Viruses ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 187
Author(s):  
Liujun Zhang ◽  
Wen Li ◽  
Yangyang Sun ◽  
Linghao Kong ◽  
Pengli Xu ◽  
...  
Keyword(s):  
Virus Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Respiratory Syndrome Virus ◽  
Interferon Α ◽  
Fc Gamma Receptor ◽  
Gamma Receptor ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Antibody-dependent enhancement (ADE) contributes to the pathogenesis of porcine reproductive and respiratory syndrome virus (PRRSV)-persistent infection. However, the mechanisms of PRRSV-ADE infection are still confusing. A clear understanding of the event upon virus infection by the ADE pathway has become crucial for developing efficient intervention of the PRRSV infection. In this study, an ADE assay showed that PRRSV-ADE infection in porcine alveolar macrophages (AMs) significantly decreased the production of interferon-α (IFN-α) and tumor necrosis factor-α (TNF-α), and significantly increased the production of interleukine-10 (IL-10). A gene knockdown assay based on small interfering RNA (siRNA) showed that both Fc gamma receptor I (FcγRI) and FcγRIII in porcine AMs were involved in PRRSV-ADE infection. An activation assay showed that specific activation of FcγRI or FcγRIII in porcine AMs during PRRSV infection not only significantly decreased the production of IFN-α and TNF-α, but also significantly increased the production of IL-10 and significantly facilitated PRRSV replication. In conclusion, our studies suggested that ADE downregulated the production of IFN-α and TNF-α in porcine AMs maybe via FcγRI and FcγRIII, thereby leading to enhanced PRRSV infection.

Study on the Anti-Gout Activity of Chlorogenic Acid: Improvement on Hyperuricemia and Gouty Inflammation

2014 ◽  
Vol 42 (06) ◽  
pp. 1471-1483 ◽  
Author(s):  
Zhao-Qing Meng ◽  
Zhao-Hui Tang ◽  
Yun-Xia Yan ◽  
Chang-Run Guo ◽  
Liang Cao ◽  
...  
Keyword(s):  
Uric Acid ◽  
Chlorogenic Acid ◽  
Gouty Arthritis ◽  
Monosodium Urate ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Factor Α ◽  
Anti Inflammation ◽  
Necrosis Factor ◽  
Msu Crystals

Gout is a metabolic disorder associated with hyperuricemia resulting in the deposition of monosodium urate (MSU) crystals in joints and tissues. Lowering serum uric acid (Sur) levels and anti-inflammation are highly essential in treating gout. Chlorogenic acid (CA), as one of the most abundant polyphenols in the Chinese medicines, has been rarely reported to have an anti-gout effect. The model of potassium oxonate (PO)-induced hyperuricemia in mice and MSU crystal-induced inflammation in rats has been established in this study. The potential beneficial effects and mechanisms of CA on hyperuricemia and gouty arthritis were elucidated. The results demonstrated that CA significantly decreased the Sur level by inhibiting the xanthine oxidase (XOD) activity but not increasing the urinary uric acid (Uur) level. In addition, CA also exhibited the effect of suppressing paw swelling. Further investigation indicated that CA improved the symptoms of inflammation induced by MSU crystals by inhibiting the production of proinflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). The present study suggests that CA may have a considerable potential for development as an anti-gouty arthritis agent for clinical application.

scholarly journals Particle size and activation threshold: a new dimension of danger signaling

Blood ◽  
2010 ◽  
Vol 115 (22) ◽  
pp. 4533-4541 ◽  
Author(s):  
Lorna Rettig ◽  
Sebastian P. Haen ◽  
Anne Greet Bittermann ◽  
Lotta von Boehmer ◽  
Alessandra Curioni ◽  
...  
Keyword(s):  
Immune Cells ◽  
Interferon Α ◽  
Innate Response ◽  
Activation Threshold ◽  
Tnf Α ◽  
Nanometric Particles ◽  
Human Immune ◽  
Factor Α ◽  
Molecular Patterns ◽  
Necrosis Factor

Abstract Previous studies have shown that single-stranded RNA (ssRNA) mixed with protamine forms particles and activates immune cells through Toll-like receptors (TLRs). We have found that the size of protamine-RNA particles generated depends on the electrolyte content when mixing the 2 components. Moreover, we have evidenced that (1) nanometric particles induce production of interferon-α, whereas (2) micrometric particles mainly induce production of tumor necrosis factor-α (TNF-α) in human immune cells. We found that the mechanisms underlying these observations are (1) nanoparticles but not microparticles are selectively phagocytosed by plasmacytoid dendritic cells (pDCs), which produce interferon-α and (2) monocytes that produce TNF-α have a higher activation threshold than that of pDCs. Thus, at the same time as sensing pathogen-associated molecular patterns such as ssRNA, the immune system distinguishes the size of the associated structure in such a way as to trigger the adapted antivirus (nanometric) or antibacterial/antifungal (micrometric) immune response. Our results introduce a new dimension in danger signaling—how size qualitatively affects innate response.

scholarly journals Isolation and Characterization of the Fungal Metabolite 3-O-Methylviridicatin as an Inhibitor of Tumour Necrosis Factor α-Induced Human Immunodeficiency Virus Replication

1998 ◽  
Vol 9 (2) ◽  
pp. 149-155 ◽  
Author(s):  
A Heguy ◽  
P Cai ◽  
P Meyn ◽  
D Houck ◽  
S Russo ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cell Line ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Luciferase Reporter ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Factor Α ◽  
Necrosis Factor

The cytokine tumour necrosis factor α (TNF-α) has been shown to play a role in human immunodeficiency virus (HIV) replication by activating transcription of the provirus in both T cells and macrophages. Therefore, agents that block TNF-α-induced HIV expression could have therapeutic value in the treatment of AIDS. We have sought to identify antiviral agents that block TNF-α induction of HIV LTR-directed transcription, using a cell-based, virus-free assay system in automated high-throughput screening. HeLa cells were transfected with an HIV LTR–luciferase reporter plasmid and a stable line was isolated in which TNF-α increased luciferase production by two- to threefold. This cell line was used to screen approximately 15 000 fungal extracts. An inhibitory activity specific for TNF-α-induced HIV LTR transcription was observed in culture OS-F67406. The active component was isolated and identified as a known metabolite, 3-O-methylviridicatin, by NMR and mass spectrometry. No biological activity has been associated with this compound previously. This compound blocks TNF-α activation of the HIV LTR in the HeLa-based system, with an IC50 of 5 μM, and inhibited virus production in the OM-10.1 cell line, a model of chronic infection responsive to induction by TNF-α, with an IC50 of 2.5 μM.

Response of hairy cells to IFN-α involves induction of apoptosis through autocrine TNF-α and protection by adhesion

Blood ◽  
2002 ◽  
Vol 100 (2) ◽  
pp. 647-653 ◽  
Author(s):  
Peter K. Baker ◽  
Andrew R. Pettitt ◽  
Joseph R. Slupsky ◽  
Hai J. Chen ◽  
Mark A. Glenn ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Interferon Α ◽  
The Novel ◽  
Tnf Α ◽  
Hairy Cells ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Blocking Antibodies ◽  
Biologic Basis ◽  
Necrosis Factor

Abstract Although hairy cell leukemia is uniquely sensitive to interferon-α (IFN-α), the biologic basis for this phenomenon remains unclear. Here we examine the effects of IFN-α on cultured hairy cells (HCs), taking into account the possible modifying influence of cell adhesion. We make the novel observation that therapeutic concentrations of IFN-α kill nonadherent HCs by inducing apoptosis. In keeping with the persistence of HCs in tissues during therapy, such killing was inhibited by integrin-mediated adhesion to vitronectin or fibronectin. Exposure of HCs to IFN-α resulted in a marked increase in tumor necrosis factor-α (TNF-α) secretion. Furthermore, blocking antibodies to TNF-RI or TNF-RII protected HCs from IFN-α–induced apoptosis, demonstrating that such killing was mediated by TNF-α. In the absence of IFN-α, exogenous TNF-α did not induce HC apoptosis, showing that IFN-α sensitized HCs to the proapoptotic effect of autocrine TNF-α. This sensitization to TNF-α–induced killing was attributable to suppression of IAP (inhibitors of apoptosis) production known to be regulated by the cytoprotective nuclear factor–κB–dependent arm of TNF-α signaling. Moreover, engagement of the receptors for fibronectin or vitronectin prevented this IFN-α–induced down-regulation of IAPs. Understanding of the signals involved in the combined effects of IFN-α and TNF-α and abrogation of those induced by integrin engagement offers the possibility of sensitizing other malignant cells to IFN-α–induced killing and thereby extending the therapeutic use of this cytokine.

scholarly journals Beneficial effects of ROCEN (Topical Nano-arthrocen) on atopic dermatitis in mice

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ramin Goudarzi ◽  
Maryam Eskandarynasab ◽  
Ahad Muhammadnejad ◽  
Ahmad Reza Dehpour ◽  
Alireza Partoazar
Keyword(s):  
Atopic Dermatitis ◽  
Topical Administration ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Leucocyte Infiltration ◽  
Histological Indices ◽  
Skin Healing ◽  
Factor Α ◽  
Necrosis Factor

Abstract Objective Atopic dermatitis (AD) is a chronic inflammatory skin disease mainly caused by immune stimuli. The current study was conducted to investigate the effects of ROCEN and to compare it with betamethasone (Beta) on mice subjected to AD. Methods First, the safety of topical ROCEN was tested to determine possible sensitization induction in vivo. Then, the mice were subjected to oxazolone (Oxa) to induce chronic AD. Consequently, they underwent treatment with ROCEN and Beta. Scratching and wiping behaviors related to dermatitis were evaluated in treated animals for 35 days. The histopathology and immunohistochemistry (IHC) analysis of interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) cytokines were performed on the dorsal skin of the treated mice. Results Topical administration of ROCEN and Beta to the dorsum of sensitized mice for 5 weeks significantly alleviated scratching and wiping symptoms and reduced erythema, scaling, and edema in the skin of the mice with AD. Moreover, histological indices showed that ROCEN effectively reduced leucocyte infiltration and improved skin healing parameters in treated AD mice. Application of ROCEN or Beta reduced IHC markers including IL-8 and TNF-α significantly. Conclusion ROCEN alleviated the AD symptoms similar to betamethasone in an experimental animal model.

The Tumor Necrosis Factor-α-blocking Agent Infliximab Inhibits Interleukin 1ß (IL-1ß) and IL-6 Gene Expression in Human Osteoblastic Cells

2009 ◽  
Vol 36 (8) ◽  
pp. 1575-1579 ◽  
Author(s):  
ESTELLA MUSACCHIO ◽  
CHIARA VALVASON ◽  
CONSTANTIN BOTSIOS ◽  
FRANCESCA OSTUNI ◽  
ANTONIO FURLAN ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Rheumatic Diseases ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Infliximab Treatment ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective.Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine involved in the pathogenesis of several rheumatic diseases, including rheumatoid arthritis (RA), associated with systemic bone loss and subchondral bone erosions. TNF-α-blocking agents such as infliximab have been successful in treatment of disease-modifying antirheumatic drug-resistant rheumatic diseases. Infliximab therapy in RA also had beneficial effects on local bone destruction and bone mineral density. We assessed effects of infliximab treatment on the bone tissue compartment and cytokine profile expression in vitro.Methods.Osteoblast-like cells were exposed for 24 h to sera of RA patients collected at baseline and after 1 month (T1) and 3 years (T2) of infliximab treatment. Total RNA was extracted, and expression of interleukin 1ß (IL-1ß), IL-6, and osteoprotegerin (OPG) was measured by RT-PCR.Results.IL-1ß gene expression was significantly reduced by the T1 serum, and the same decrease was elicited by the T2 serum. IL-6 downregulation was evident with the T2 serum. OPG was unaffected.Conclusion.The finding of downregulation of inflammatory cytokines was interesting, particularly IL-6, which plays a crucial role in arthritis-related bone loss due to its involvement in osteoclast recruitment and activation. These results may represent a biological explanation and a link for the clinical observation of the beneficial effects of anti-TNF-α agents on the progression of rheumatic diseases at the bone level.

scholarly journals Histoplasmosis in Patients With Cell-Mediated Immunodeficiency: Human Immunodeficiency Virus Infection, Organ Transplantation, and Tumor Necrosis Factor-α Inhibition

2015 ◽  
Vol 2 (1) ◽  
Author(s):  
Keith Luckett ◽  
J. Stephen Dummer ◽  
Geraldine Miller ◽  
Sydney Hester ◽  
Lora Thomas
Keyword(s):  
Human Immunodeficiency Virus ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Severe Disease ◽  
Initial Therapy ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background.  Histoplasmosis causes severe disease in patients with defects of cell-mediated immunity. It is not known whether outcomes vary related to the type of immunodeficiency or class of antifungal treatment. Methods.  We reviewed cases of active histoplasmosis that occurred at Vanderbilt University Medical Center from July 1999 to June 2012 in patients with human immunodeficiency virus (HIV) infection, a history of transplantation, or tumor necrosis factor (TNF)-α inhibitor use. These groups were compared for differences in clinical presentation and outcomes. In addition, outcomes were related to the initial choice of treatment. Results.  Ninety cases were identified (56 HIV, 23 transplant, 11 TNF-α inhibitor). Tumor necrosis factor-α patients had milder disease, shorter courses of therapy, and fewer relapses than HIV patients. Histoplasma antigenuria was highly prevalent in all groups (HIV 88%, transplant 95%, TNF-α 91%). Organ transplant recipients received amphotericin B formulation as initial therapy less often than other groups (22% vs 57% HIV vs 55% TNF-α; P = .006). Treatment failures only occurred in patients with severe disease. The failure rate was similar whether patients received initial amphotericin or triazole therapy. Ninety-day histoplasmosis-related mortality was 9% for all groups and did not vary significantly with choice of initial treatment. Conclusions.  Histoplasmosis caused milder disease in patients receiving TNF-α inhibitors than patients with HIV or solid organ transplantation. Treatment failures and mortality only occurred in patients with severe disease and did not vary based on type of immunosuppression or choice of initial therapy.

scholarly journals Beneficial Effects of Liposome Containing Arthrocen (ROCEN)) on Atopic Dermatitis in Mice

2021 ◽  
Author(s):  
Ramin Goudarzi ◽  
Maryam Eskandarynasab ◽  
Ahad Muhammadnejad ◽  
Ahmad Reza Dehpour ◽  
Alireza Partoazar
Keyword(s):  
Atopic Dermatitis ◽  
Beneficial Effects ◽  
Immunohistochemistry Analysis ◽  
Tnf Α ◽  
Leucocyte Infiltration ◽  
Histological Indices ◽  
Skin Healing ◽  
Factor Α ◽  
Cutaneous Administration ◽  
Necrosis Factor

Abstract Objective: Atopic dermatitis (AD) is a chronic inflammatory skin disease caused mainly by the immune stimulus. The current study aimed to investigate the effects of liposome containing arthrocen (ROCEN) and its comparison with betamethasone (Beta) on mice subjected to AD. Methods: First of all, the risk assessment of ROCEN sensitization was done, then mice were subjected to oxazolone (Oxa) for chronic AD induction and treatment. Scratching and wiping behaviors related to dermatitis were evaluated in animals treated topically with ROCEN. The histological and immunohistochemistry analysis of interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) were conducted to the dorsal skin of treated rats. Results: The results showed that cutaneous administration of ROCEN on sensitized mice for 5 weeks, alleviated significantly scratching and wiping symptoms, erythema, scaling, and edema in animals’ skin. Moreover, histological indices showed that ROCEN reduced effectively leucocyte infiltration and improved skin healing parameters in AD mice. Immunohistochemically markers of IL-8 and TNF-α were hindered significantly by ROCEN in dermal tissues of mice. Conclusion: ROCEN potentiated alleviation of the AD symptoms rather than betamethasone drug in an experimental model.

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