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Steroid-Induced Diabetes Ketoacidosis in an Immune Thrombocytopenia Patient: A Case Report and Literature Review.
Alakkas, Z, Alzaedi, OA, Somannavar, SS, Alfaifi, A
The American journal of case reports. 2020;:e923372
Abstract
BACKGROUND Steroids are used as anti-inflammatory agents, administered for a variety of medical conditions, either as short- or long-term treatment. Steroid use is associated with many adverse effects, including hyperglycemia, but ketoacidosis is rare. CASE REPORT We present the case of a 53-year-old woman who developed diabetic ketoacidosis after administration of methylprednisolone during treatment of immune thrombocytopenic purpura. She did not have diabetes or a family history of diabetes. Steroid-induced hyperglycemia with insulin resistance, lipolysis, and ketogenesis occurred and were likely to have precipitated the ketoacidosis. Blood glucose, blood gases, and urine test results were diagnostic for ketoacidosis. CONCLUSIONS The risk of ketoacidosis and hyperglycemia should be considered in the course of steroid therapy, even without a diagnosis of diabetes, especially in patients who have risk factors for diabetes mellitus including obesity and long-term use of steroids, so that early identification of diabetic ketoacidosis can prevent further morbidity and mortality in chronic patients.
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Evaluation of mechanisms of action of re-purposed drugs for treatment of COVID-19.
Rajaiah, R, Abhilasha, KV, Shekar, MA, Vogel, SN, Vishwanath, BS
Cellular immunology. 2020;:104240
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Coronavirus disease 2019 (COVID-19) is a global health emergency caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). The rapid worldwide spread of SARS-CoV-2 infection has necessitated a global effort to identify effective therapeutic strategies in the absence of vaccine. Among the re-purposed drugs being tested currently, hydroxychloroquine (HCQ), without or with zinc ion (Zn++) and the antibiotic azithromycin (AZM), has been administered to prevent or treat patients with COVID-19. The outcome of multiple clinical studies on HCQ has been mixed. Zn++ interferes with viral replication by inhibiting replicative enzymes and its entry into cells may be facilitated by HCQ. Another immunomodulatory drug, methotrexate (MTX), is well known for its ability to mitigate overactive immune system by upregulating the anti-inflammatory protein, A20. However, its beneficial effect in treating COVID-19 has not drawn much attention. This review provides an overview of the virology of SARS-CoV-2 and an analysis of the mechanisms by which these anti-inflammatory agents may act in the treatment of COVID-19 patients. We propose a rationale for the combinatorial use of these re-purposed drugs that may help to combat this ongoing pandemic health emergency.
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Targeting immunometabolism as an anti-inflammatory strategy.
Pålsson-McDermott, EM, O'Neill, LAJ
Cell research. 2020;(4):300-314
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The growing field of immunometabolism has taught us how metabolic cellular reactions and processes not only provide a means to generate ATP and biosynthetic precursors, but are also a way of controlling immunity and inflammation. Metabolic reprogramming of immune cells is essential for both inflammatory as well as anti-inflammatory responses. Four anti-inflammatory therapies, DMF, Metformin, Methotrexate and Rapamycin all work by affecting metabolism and/or regulating or mimicking endogenous metabolites with anti-inflammatory effects. Evidence is emerging for the targeting of specific metabolic events as a strategy to limit inflammation in different contexts. Here we discuss these recent developments and speculate on the prospect of targeting immunometabolism in the effort to develop novel anti-inflammatory therapeutics. As accumulating evidence for roles of an intricate and elaborate network of metabolic processes, including lipid, amino acid and nucleotide metabolism provides key focal points for developing new therapies, we here turn our attention to glycolysis and the TCA cycle to provide examples of how metabolic intermediates and enzymes can provide potential novel therapeutic targets.
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Lactoferrin as potential preventative and adjunct treatment for COVID-19.
Chang, R, Ng, TB, Sun, WZ
International journal of antimicrobial agents. 2020;(3):106118
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The coronavirus disease 2019 (COVID-19) pandemic is rapidly advancing across the globe despite drastic public and personal health measures. Antivirals and nutritional supplements have been proposed as potentially useful against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus that causes COVID-19, but few have been clinically established. Lactoferrin (Lf) is a naturally occurring, non-toxic glycoprotein that is orally available as a nutritional supplement and has established in vitro antiviral efficacy against a wide range of viruses, including SARS-CoV, a closely related coronavirus to SARS-CoV-2. Furthermore, Lf possesses unique immunomodulatory and anti-inflammatory effects that may be especially relevant to the pathophysiology of severe COVID-19 cases. Here we review the underlying biological mechanisms of Lf as an antiviral and immune regulator, and propose its unique potential as a preventative and adjunct treatment for COVID-19. We hope that further research and development of Lf nutritional supplementation would establish its role for COVID-19.
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Anti-Inflammatory Activity of Extracts and Pure Compounds Derived from Plants via Modulation of Signaling Pathways, Especially PI3K/AKT in Macrophages.
Merecz-Sadowska, A, Sitarek, P, Śliwiński, T, Zajdel, R
International journal of molecular sciences. 2020;(24)
Abstract
The plant kingdom is a source of important therapeutic agents. Therefore, in this review, we focus on natural compounds that exhibit efficient anti-inflammatory activity via modulation signaling transduction pathways in macrophage cells. Both extracts and pure chemicals from different species and parts of plants such as leaves, roots, flowers, barks, rhizomes, and seeds rich in secondary metabolites from various groups such as terpenes or polyphenols were included. Selected extracts and phytochemicals control macrophages biology via modulation signaling molecules including NF-κB, MAPKs, AP-1, STAT1, STAT6, IRF-4, IRF-5, PPARγ, KLF4 and especially PI3K/AKT. Macrophages are important immune effector cells that take part in antigen presentation, phagocytosis, and immunomodulation. The M1 and M2 phenotypes are related to the production of pro- and anti-inflammatory agents, respectively. The successful resolution of inflammation mediated by M2, or failed resolution mediated by M1, may lead to tissue repair or chronic inflammation. Chronic inflammation is strictly related to several disorders. Thus, compounds of plant origin targeting inflammatory response may constitute promising therapeutic strategies.
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Mediterranean Diet: Lipids, Inflammation, and Malaria Infection.
Silva, AR, Moraes, BPT, Gonçalves-de-Albuquerque, CF
International journal of molecular sciences. 2020;(12)
Abstract
The Mediterranean diet (MedDiet) consists of consumption of vegetables and healthy oils and have beneficial effects on metabolic and inflammatory diseases. Our goal here is to discuss the role of fatty acid content in MedDiet, mostly omega-3, omega-6, and omega-9 on malaria. Malaria affects millions of people around the globe. The parasite Plasmodium causes the disease. The metabolic and inflammatory alterations in the severe forms have damaging consequences to the host. The lipid content in the MedDiet holds anti-inflammatory and pro-resolutive features in the host and have detrimental effects on the Plasmodium. The lipids from the diet impact the balance of pro- and anti-inflammation, thus, lipids intake from the diet is critical to parasite elimination and host tissue damage caused by an immune response. Herein, we go into the cellular and molecular mechanisms and targets of the MedDiet fatty acids in the host and the parasite, reviewing potential benefits of the MedDiet, on inflammation, malaria infection progression, and clinical outcome.
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Critical roles of inflammation in atherosclerosis.
Moriya, J
Journal of cardiology. 2019;(1):22-27
Abstract
There is accumulating evidence that vascular inflammation plays critical roles in pathophysiology of atherosclerosis. It is widely accepted that both innate and adaptive immune responses are important for initiation and progression of atherosclerosis, which mainly consist of monocytes, macrophages, neutrophils, T lymphocytes, and B lymphocytes. Moreover, inflammatory biomarkers such as high-sensitivity C-reactive protein and interleukin-6 are known to predict future cardiovascular events, as well as conventional low-density or high-density lipoprotein cholesterol. Thus, current understanding of the inflammatory mechanisms of atherosclerosis have led us to explore novel therapeutic approaches that reducing vascular inflammation itself could lower the rates of critical cardiovascular events. To address the inflammatory hypothesis of atherosclerosis, results of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) trial have been recently reported that anti-inflammatory therapy using canakinumab, a monoclonal antibody targeting interleukin-1β, significantly reduced recurrent cardiovascular events for secondary prevention of myocardial infarction at high inflammatory risk. In this review, we will first outline the mechanisms of atherosclerosis, especially focusing on their inflammatory aspects. Then we will introduce several critical inflammatory biomarkers that contribute to risk stratification of clinical cardiovascular events. Lastly, we will discuss potentiality and future perspectives of reducing inflammation as a novel therapeutic target for atherosclerotic cardiovascular diseases.
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Vortioxetine exerts anti-inflammatory and immunomodulatory effects on human monocytes/macrophages.
Talmon, M, Rossi, S, Pastore, A, Cattaneo, CI, Brunelleschi, S, Fresu, LG
British journal of pharmacology. 2018;(1):113-124
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BACKGROUND AND PURPOSE A crosstalk between the immune system and depression has been postulated, with monocytes/macrophages and cytokines having a key role in this interaction. In this study, we examined whether vortioxetine, a multimodal anti-depressive drug, was endowed with anti-inflammatory and antioxidative activity, leading to immunomodulatory effects on human monocytes and macrophages. EXPERIMENTAL APPROACH Human monocytes were isolated from buffy coats and used as such or differentiated into M1 and M2 macrophages. Cells were treated with vortioxetine before or after differentiation, and their responsiveness was evaluated. This included oxy-radical and TNFα production, TNFα and PPARγ gene expression and NF-κB translocation. KEY RESULTS Vortioxetine significantly reduced the PMA-induced oxidative burst in monocytes and in macrophages (M1 and M2), causing a concomitant shift of macrophages from the M1 to the M2 phenotype, demonstrated by a significant decrease in the expression of the surface marker CD86 and an increase in CD206. Moreover, treatment of monocytes with vortioxetine rendered macrophages derived from this population less sensitive to PMA, as it reduced the oxidative burst, NF-kB translocation, TNFα release and expression while inducing PPARγ gene expression. FACS analysis showed a significant decrease in the CD14+ /CD16+ /CD86+ M1 population. CONCLUSIONS AND IMPLICATIONS These results demonstrate that in human monocytes/macrophages, vortioxetine has antioxidant activity and anti-inflammatory effects driving the polarization of macrophages towards their alternative phenotype. These findings suggest that vortioxetine, alongside its antidepressive effect, may have immunomodulatory properties.
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Prediction of anti-inflammatory proteins/peptides: an insilico approach.
Gupta, S, Sharma, AK, Shastri, V, Madhu, MK, Sharma, VK
Journal of translational medicine. 2017;(1):7
Abstract
BACKGROUND The current therapy for inflammatory and autoimmune disorders involves the use of nonspecific anti-inflammatory drugs and other immunosuppressant, which are often accompanied with potential side effects. As an alternative therapy, anti-inflammatory peptides are recently being exploited as anti-inflammatory agents for treatment of various inflammatory diseases such as Alzheimer's disease and rheumatoid arthritis. Thus, understanding the correlation between amino acid sequence and its potential anti-inflammatory property is of great importance for the discovery of novel and efficient anti-inflammatory peptide-based therapeutics. METHODS In this study, we have developed a prediction tool for the classification of peptides as anti-inflammatory epitopes or non anti-inflammatory epitopes. The training was performed using experimentally validated epitopes obtained from Immune epitope database and analysis resource database. Different sequence-based features and their hybrids with motif information were employed for development of support vector machine-based machine learning models. Similarly, machine learning models were also constructed using random forest. RESULTS The composition and terminal residue conservation analysis of peptides revealed the dominance of leucine, serine, tyrosine and arginine residues in anti-inflammatory epitopes as compared to non anti-inflammatory epitopes. Similarly, the anti-inflammatory epitopes specific motifs were found to be rich in hydrophobic and polar residues. The hybrid of tripeptide composition-based support vector machine model and motif yielded the best performance on 10-fold cross validation with an accuracy of 78.1% and MCC of 0.58. The same displayed an accuracy of 72% and MCC of 0.45 on validation dataset, rejecting any possibility of over-fitting. The tripeptide composition-based random forest model displayed an accuracy of 0.8 and MCC of 0.59 on 10-fold cross validation, however, the accuracy (0.68) and MCC (0.31) was lower as compared to support vector machine model on validation dataset. Thus, the support vector machine model is implemented as the default model and an additional option of using the random forest model is provided. CONCLUSION The prediction models along with tools for epitope mapping and similarity search have been provided as a web server which is freely accessible at http://metagenomics.iiserb.ac.in/antiinflam/ .