Ravneet Kaur

New York University

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Chiara Giannarelli

New York University

Letizia Amadori

New York University

Swathy Sajja

New York University

Dawn Fernandez

Albert Einstein College of Medicine

Natalia Eberhardt

New York University

Roza Shamailova

NYU Langone Health

Kathryn J. Moore

New York University

Michael Gildea

Cardiovascular Research Center

Dayasagar Das

All India Institute of Medical Sciences Bhopal

Edward A. Fisher

Cardiovascular Research Center

Cooperative Institutions

New York University

Icahn School of Medicine at Mount Sinai

NYU Langone Health

Hinge Health

Columbia University Irving Medical Center

Post Graduate Institute of Medical Education and Research

Cardiovascular Research Center

Mount Sinai Health System

All India Institute of Medical Sciences

Columbia University

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Loss of PRMT2 in myeloid cells in normoglycemic mice phenocopies impaired regression of atherosclerosis in diabetic mice

Scientific Reports (2022)

Beyza Vurusaner Prashanth Thevkar-Nages Ravneet Kaur Chiara Giannarelli Michael J. Garabedian

Abstract The regression, or resolution, of inflammation in atherosclerotic plaques is impaired in diabetes. However, the factors mediating this effect remain incomplete. We identified protein arginine methyltransferase 2 (PRMT2) as a protein whose expression in macrophages is reduced in hyperglycemia and diabetes. PRMT2 catalyzes arginine methylation to target proteins to modulate gene expression. Because PRMT2 expression is reduced in cells in hyperglycemia, we wanted to determine whether PRMT2 plays a causal role in the impairment of atherosclerosis regression in diabetes. We, therefore, examined the consequence of deleting PRMT2 in myeloid cells during the regression of atherosclerosis in normal and diabetic mice. Remarkably, we found significant impairment of atherosclerosis regression under normoglycemic conditions in mice lacking PRMT2 ( Prmt2 −/− ) in myeloid cells that mimic the decrease in regression of atherosclerosis in WT mice under diabetic conditions. This was associated with increased plaque macrophage retention, as well as increased apoptosis and necrosis. PRMT2-deficient plaque CD68+ cells under normoglycemic conditions showed increased expression of genes involved in cytokine signaling and inflammation compared to WT cells. Consistently, Prmt2 −/− bone marrow-derived macrophages (BMDMs) showed an increased response of proinflammatory genes to LPS and a decreased response of inflammation resolving genes to IL-4. This increased response to LPS in Prmt2 −/− BMDMs occurs via enhanced NF-kappa B activity. Thus, the loss of PRMT2 is causally linked to impaired atherosclerosis regression via a heightened inflammatory response in macrophages. That PRMT2 expression was lower in myeloid cells in plaques from human subjects with diabetes supports the relevance of our findings to human atherosclerosis.

10.1038/s41598-022-15349-6

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Role of Gandhaka Rasayana along with Karpoor mixed Nimba taila in the treatment of Dadru - Case Report

International Journal of Ayurvedic Medicine (2022)

Jasmine Sudhir Kumar Pani Vishal Prajapati Shashidhar Kumar Ravneet Kaur

From the ancient time and till date of modern era, skin plays important role in all over the self-confidence and mental health. The first thing whenever we see person is skin as skin is the largest organ of body. If person suffering from any skin disease specially in face. Then it appears irritable and give negative impact on self-confidence and mental health. Every person in the world wants to be more beautiful than anyone. In this case study, A patient suffered from dadru on thigh region have treated. In dadru, elevated skin lesions with rashes, itching and redness associated with burning sensation appears with circular shape. All Acharyas mentioned all skin disease under kushtha. There are two types of kushtha, mahakushtha and kshudra kushtha mentioned in Ayurveda. Acharya Charak mentioned dadru into kshudra kushtha but Acharya Sushrut explained it into maha kushtha. Nidan and samprapti of all the kushtha types are same. We can correlate dadru with Tinea corporis as they have similar properties and appearance. In the present case study Karpoor mix Nimba taila was applied locally to the affected area of patient and Gandhak rasayan orally for 7days. Patient got completely relief from dadru on seventh day of treatment. This study showed that local application of Karpoor mixed with Nimba taila and orally Gandhak rasayan shows significant efficacy in the management of dadru.

Itching

10.47552/ijam.v13i2.1829

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Inspite of controversy in Girisindoora, Naagsindoora, and Rasanjna, their safe use in eye diseases

International journal of advance research, ideas and innovations in technology (2018)

Ravneet Kaur

An attempt is made to overview safety of these controversial medicines i.e. Girisindoora, Naagsindoora, rasanjna in eye diseases. Girisindoora and Rafsanjani are classified in Sadharana Rasa Varga and Naagsindoora is described in Dhatu Varga (metallic group). Chemically these are different from each other but some authors said they are alike. Girisindoora is an oxide of mercury (HgO), Naagsindoora is Lead peroxide (PbO) and rasanjna is the mercuric oxide (HgO). These all can be used safely in eye diseases in spite of controversies regarding their availability and similarity.

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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Natalia Eberhardt María G. Noval Ravneet Kaur Swathy Sajja Letizia Amadori

COVID-19 patients present higher risk for myocardial infarction (MI), acute coronary syndrome, and stroke for up to 1 year after SARS-CoV-2 infection. While the systemic inflammatory response to SARS-CoV-2 infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques to locally promote inflammation remains unknown. Here, we report that SARS-CoV-2 viral RNA (vRNA) is detectable and replicates in coronary atherosclerotic lesions taken at autopsy from patients with severe COVID-19. SARS-CoV-2 localizes to plaque macrophages and shows a stronger tropism for arterial lesions compared to corresponding perivascular fat, correlating with the degree of macrophage infiltration. In vitro infection of human primary macrophages highlights that SARS-CoV-2 entry is increased in cholesterol-loaded macrophages (foam cells) and is dependent, in part, on neuropilin-1 (NRP-1). Furthermore, although viral replication is abortive, SARS-CoV-2 induces a robust inflammatory response that includes interleukins IL-6 and IL-1β, key cytokines known to trigger ischemic cardiovascular events. SARS-CoV-2 infection of human atherosclerotic vascular explants recapitulates the immune response seen in cultured macrophages, including pro-atherogenic cytokine secretion. Collectively, our data establish that SARS-CoV-2 infects macrophages in coronary atherosclerotic lesions, resulting in plaque inflammation that may promote acute CV complications and long-term risk for CV events.

10.1101/2023.08.14.553245

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Response to “Postoperative atrial fibrillation after thoracic surgery: addressing risk factors and outcomes”—a letter to the Editor

The Cardiothoracic Surgeon (2023)

Kanakath Sanvi Ravneet Kaur

Cardiothoracic surgery

10.1186/s43057-023-00116-8

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A homoeopathic approach to inflammatory bowel disease (IBD)

International Journal of Homoeopathic Sciences (2022)

Amritpreet Kaur Ravneet Kaur

Inflammatory bowel disease (IBD) is defined as chronic inflammation of intestines both large intestine and small intestine that results from genetic factors, environmental factors and immunological factors. Inflammatory bowel disease (IBD) comprises of two major forms, that are known as Ulcerative colitis and Crohn’s disease. The clinical presentation of IBD are pain in abdominal region, diarrhoea, blood-stained stools and vomiting. In most of the cases of IBD, intestinal epithelial barrier function were predicted defected. In this review, we first describe both forms of Inflammatory bowel disease(IBD) that are Ulcerative colitis and Crohn’s disease with complete symptomatology and investigations along with rubrics and homoeopathic management.

10.33545/26164485.2022.v6.i2b.544

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Abstract 13609: Heterogeneous Populations of Cytotoxic CD4 T Cells Are Expanded in Atherosclerotic Plaques of Patients With Type 2 Diabetes

Circulation (2022)

Dayasagar Das Ravneet Kaur Michael Gildea Natalia Eberhardt Dawn Fernandez

Introduction: Atherosclerotic cardiovascular disease (ACVD) is the main cause of morbidity and mortality in patients with type 2 diabetes (T2D). ACVD is more severe and diffuse in T2D than in subjects with no diabetes (ND). Moreover, cholesterol reduction in T2D leads to less plaques resolution. While the role of macrophages in T2D plaque pathology has been investigated, no studies have systematically investigated the heterogeneity of CD4 T cells in human plaques. Hypothesis: Plaques of patients with T2D have a greater CD4 T cell heterogeneity and pathogenic phenotypes compared with plaques of ND subjects. Methods: To identify the specific T cell alterations in plaques we analyzed scRNA sequencing data of >80,000 plaque immune cells from 22 patients undergoing carotid endarterectomy with or without T2D (54.5% T2D). Results: Unbiased clustering of CD45+ cells identified a total of 24 immune cell clusters, including CD4 T cells that presented similar cell frequencies between T2D (~11%) and ND patients (~10%). CD4 T cells comprise 7 clusters: naïve, proliferating, central memory (CM), effector memory (EM), T regulatory (Tregs), cytotoxic (CTL), and gamma delta (γδ) T cells. CD4 CTLs expressed GZMB, GNLY, PRF1 , and could be divided into TRAC +EM (cluster 9) and CTLγδ T cells expressing both TRDC and TRGC2 (cluster 5). CTLγδ T cells were significantly expanded in T2D plaques (p=0.032), and expressed high levels of GZMA and transcription factors involved in T cell differentiation such as RUNX and TBX21 . These CTLγδ T cells are enriched with sets of genes involved in T-cell activation, numerous pathways of apoptosis, cytotoxicity, chemotaxis and cytokine signaling (i.e. IL1, IL2, IL9 ). Conclusions: Our data show that plaques from patients with T2D are highly enriched in unique CTL/γδ T cells and suggest that their cytotoxic potential may contribute to the increased cardiovascular risk of subjects with T2D.

CTL*

10.1161/circ.146.suppl_1.13609

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Infections Associated Hemophagocytosis-Secondary HLH Mimics in Children!”

Indian Journal of Hematology and Blood Transfusion (2022)

Bhavika Rishi Aroonima Misra Ravneet Kaur Varsha Mishra Sonal Jain

Hemophagocytosis

Hematology

10.1007/s12288-022-01577-3

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The IRG1–itaconate axis protects from cholesterol-induced inflammation and atherosclerosis

Proceedings of the National Academy of Sciences (2024)

Yannick Cyr Fazli Bozal José Gabriel Barcia Durán Alexandra Newman Letizia Amadori

Atherosclerosis is fueled by a failure to resolve lipid-driven inflammation within the vasculature that drives plaque formation. Therapeutic approaches to reverse atherosclerotic inflammation are needed to address the rising global burden of cardiovascular disease (CVD). Recently, metabolites have gained attention for their immunomodulatory properties, including itaconate, which is generated from the tricarboxylic acid-intermediate cis-aconitate by the enzyme Immune Responsive Gene 1 (IRG1/ACOD1). Here, we tested the therapeutic potential of the IRG1–itaconate axis for human atherosclerosis. Using single-cell RNA sequencing (scRNA-seq), we found that IRG1 is up-regulated in human coronary atherosclerotic lesions compared to patient-matched healthy vasculature, and in mouse models of atherosclerosis, where it is primarily expressed by plaque monocytes, macrophages, and neutrophils. Global or hematopoietic Irg1 -deficiency in mice increases atherosclerosis burden, plaque macrophage and lipid content, and expression of the proatherosclerotic cytokine interleukin (IL)-1β. Mechanistically, absence of Irg1 increased macrophage lipid accumulation, and accelerated inflammation via increased neutrophil extracellular trap (NET) formation and NET-priming of the NLRP3-inflammasome in macrophages, resulting in increased IL-1β release. Conversely, supplementation of the Irg1 –itaconate axis using 4-octyl itaconate (4-OI) beneficially remodeled advanced plaques and reduced lesional IL-1β levels in mice. To investigate the effects of 4-OI in humans, we leveraged an ex vivo systems-immunology approach for CVD drug discovery. Using CyTOF and scRNA-seq of peripheral blood mononuclear cells treated with plasma from CVD patients, we showed that 4-OI attenuates proinflammatory phospho-signaling and mediates anti-inflammatory rewiring of macrophage populations. Our data highlight the relevance of pursuing IRG1–itaconate axis supplementation as a therapeutic approach for atherosclerosis in humans.

Proinflammatory cytokine

Foam cell

10.1073/pnas.2400675121

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Immune checkpoint landscape of human atherosclerosis and influence of cardiometabolic factors

Nature Cardiovascular Research (2024)

José Gabriel Barcia Durán Dayasagar Das Michael Gildea Letizia Amadori Morgane Gourvest

Immune checkpoint inhibitor (ICI) therapies can increase the risk of cardiovascular events in survivors of cancer by worsening atherosclerosis. Here we map the expression of immune checkpoints (ICs) within human carotid and coronary atherosclerotic plaques, revealing a network of immune cell interactions that ICI treatments can unintentionally target in arteries. We identify a population of mature, regulatory CCR7+FSCN1+ dendritic cells, similar to those described in tumors, as a hub of IC-mediated signaling within plaques. Additionally, we show that type 2 diabetes and lipid-lowering therapies alter immune cell interactions through PD-1, CTLA4, LAG3 and other IC targets in clinical development, impacting plaque inflammation. This comprehensive map of the IC interactome in healthy and cardiometabolic disease states provides a framework for understanding the potential adverse and beneficial impacts of approved and investigational ICIs on atherosclerosis, setting the stage for designing ICI strategies that minimize cardiovascular disease risk in cancer survivors. Barcia Durán, Dayasagar, et al. map the expression of immune checkpoints in human atherosclerosis and examine the influence of lipid-lowering treatments and type 2 diabetes to understand how immune checkpoint inhibitors worsen cardiovascular risk in survivors of cancer.

Immune checkpoint

10.1038/s44161-024-00563-4

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