A5018940487- Systemic Lupus Erythematosus Research
- COVID-19 Clinical Research Studies
- interferon and immune responses
- T-cell and B-cell Immunology
- Sepsis Diagnosis and Treatment
- Cytokine Signaling Pathways and Interactions
- Immune Cell Function and Interaction
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Streptococcal Infections and Treatments
- Computational Drug Discovery Methods
- Atherosclerosis and Cardiovascular Diseases
- Immune Response and Inflammation
- Dermatological and COVID-19 studies
- Peroxisome Proliferator-Activated Receptors
- Pharmacological Effects of Natural Compounds
- Neuroinflammation and Neurodegeneration Mechanisms
National Institute of Arthritis and Musculoskeletal and Skin Diseases
2022-2024
National Institutes of Health
2022-2024
Dysregulation in neutrophil extracellular trap (NET) formation and degradation may play a role the pathogenesis severity of COVID-19; however, its pediatric manifestations this disease, including multisystem inflammatory syndrome children (MIS-C) chilblain-like lesions (CLLs), otherwise known as "COVID toes," remains unclear. Studying multinational cohorts, we found that, CLLs, NETs were significantly increased serum skin. There was geographic variability prevalence MIS-C, association with...
Itaconic acid, a Krebs cycle-derived immunometabolite, is synthesized by myeloid cells in response to danger signals control inflammasome activation, type I interferon (IFN) responses, and oxidative stress. As these pathways are dysregulated systemic lupus erythematosus (SLE), we investigated the role of an itaconic acid derivative treatment established murine lupus.
The Krebs cycle enzyme aconitate decarboxylase 1 (ACOD1) mediates itaconate synthesis in monocytes and macrophages. Previously, we reported that administration of 4-octyl to lupus-prone mice abrogated immune dysregulation clinical features. In this study, explore the role endogenous ACOD1/itaconate pathway development TLR7-induced lupus (imiquimod [IMQ] model). We found that, vitro, ACOD1 was induced mouse bone marrow-derived macrophages human monocyte-derived following TLR7 stimulation....
Premature cardiovascular events in systemic lupus erythematosus (SLE) contribute to morbidity and mortality, with no effective preventive strategies described date. Immune dysregulation metabolic disturbances appear play prominent roles the induction of vascular disease SLE. The peroxisome proliferator activated receptor-gamma agonist pioglitazone (PGZ suppresses damage immune murine improves endothelial dysfunction other inflammatory diseases. We hypothesised that PGZ could improve...
Abstract Dysregulation in neutrophil extracellular trap (NET) formation and degradation may play a role the pathogenesis severity of COVID-19; however, its pediatric manifestations this disease including MIS-C chilblain-like lesions (CLL), otherwise known as “COVID toes”, remains unclear. Studying multinational cohorts, we found that, CLL, NETs were significantly increased serum skin. There was geographic variability prevalence MIS-C, association with severity. CLL samples displayed...
The Krebs cycle enzyme Aconitate Decarboxylase 1 (ACOD1) mediates itaconate synthesis in myeloid cells.. Previously, we reported that administration of 4-octyl abrogated lupus phenotype mice. Here, explore the role endogenous ACOD1/itaconate pathway development murine as well their relevance premature cardiovascular damage SLE.
Abstract Mitochondrial synthesis of itaconate by myeloid cells (monocytes and macrophages) is mediated the TCA cycle enzyme Aconitate Decarboxylase 1 (Acod1). Upregulation Acod1–itaconate pathway, occurs after activation various Toll-like receptors (TLRs) or cytokine stimulation (TNF type I Interferons). While anti-inflammatory effects Acod1 – Itaconate pathway have been previously reported (e.g. decreases in IL-6 IL-1β synthesis) contribution impairments endogenous systemic lupus...