Publications by authors named "Heather Teague"

Article Synopsis
  • Modulating SYK can influence how neutrophils respond in COVID-19 and sepsis, where they can both protect against infections and contribute to tissue damage during hyperactivation.
  • R406, a metabolite of fostamatinib, effectively inhibits key harmful neutrophil activities like NETosis and ROS generation, which are associated with severe sepsis outcomes.
  • Despite these inhibitory effects, neutrophils treated with R406 remain metabolically active and can still perform essential functions like cytokine release, phagocytosis, and migration.
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Background: Psoriasis is a chronic inflammatory condition associated with coronary artery disease risk. Uptake of oxidized low-density lipoprotein by the lectin-like low-density lipoprotein receptor-1 triggers release of the soluble extracellular domain of the receptor (sLOX-1). We sought to characterize the relationship between sLOX-1, inflammation, and coronary plaque progression in psoriasis.

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Background: s: Psoriasis is a disease of systemic inflammation associated with increased cardiometabolic risk. Epicardial adipose tissue (EAT) and thoracic adipose tissue (TAT) are contributing factors for atherosclerosis and cardiac dysfunction. We strove to assess the longitudinal impact of the EAT and TAT on coronary and cardiac characteristics in psoriasis.

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Background: Existing models of Ebola virus infection have not fully characterized the pathophysiology of shock in connection with daily virologic, clinical, and immunologic parameters. We implemented a nonhuman primate critical care model to investigate these associations.

Methods: Two rhesus macaques received a target dose of 1000 plaque-forming units of Ebola virus intramuscularly with supportive care initiated on day 3.

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To evaluate whether nicotinamide adenine dinucleotide-positive (NAD) boosting modulates adaptive immunity, primary CD4 T cells from healthy control and psoriasis subjects were exposed to vehicle or nicotinamide riboside (NR) supplementation. NR blunts interferon γ (IFNγ) and interleukin (IL)-17 secretion with greater effects on T helper (Th) 17 polarization. RNA sequencing (RNA-seq) analysis implicates NR blunting of sequestosome 1 (sqstm1/p62)-coupled oxidative stress.

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Background: Psoriasis (PSO) is a skin disorder with systemic inflammation and high coronary artery disease risk. A distinct lipid phenotype occurs in psoriasis, which is characterized by high plasma triglycerides (TGs) with typically normal or even low LDL-C. The extent to which cholesterol on LDL subfractions, such as small dense LDL-C (sdLDL-C), are associated with vulnerable coronary plaque characteristics in PSO remains elusive.

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APOA-1 is central to the high-density lipoprotein function of reverse cholesterol transport measured by cholesterol efflux capacity. Psoriasis is a systemic inflammatory disease associated with poor cholesterol efflux capacity and accelerated noncalcified coronary burden (NCB) as measured by coronary computed tomographic angiography. In this study, we characterized the relationship between APOA-1, cholesterol efflux capacity, and progression of NCB over 4 years.

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Article Synopsis
  • Persistent skin inflammation leads to psoriasis and related health issues, with omega-3 polyunsaturated fatty acids (PUFAs) like EPA and DHA potentially playing a role in reducing inflammation.
  • A study was conducted using a mouse model to compare the effects of EPA and DHA over 12 weeks on psoriasis-like skin inflammation, focusing on how these substances affect inflammatory markers and lipid mediators.
  • Results showed that DHA treatment was more effective in reducing inflammation and modifying specific immune responses compared to EPA, suggesting that DHA might be the preferred option for managing psoriasis.
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Background And Objective: Psoriasis is a systemic inflammatory condition with poor cholesterol transport measured by cholesterol efflux capacity (CEC) that is associated with a heightened risk of cardiovascular disease (CVD). In psoriasis patients, we sought to characterize the lipoprotein profile by size using a novel nuclear magnetic resonance algorithm in patients with low CEC compared to normal CEC.

Methods: Lipoprotein profile was assessed using the novel nuclear magnetic resonance LipoProfile-4 deconvolution algorithm.

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Metabolic conditions such as obesity and associated comorbidities are increasing in prevalence worldwide. In chronically inflamed pathologies, metabolic conditions are linked to early onset cardiovascular disease, which remains the leading cause of death despite decades of research. In recent years, studies focused on the interdependent pathways connecting metabolism and the immune response have highlighted that dysregulated cholesterol trafficking instigates an overactive, systemic inflammatory response, thereby perpetuating early development of cardiovascular disease.

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Psoriasis is a systemic inflammatory disease with an increased risk of atherosclerotic events and premature cardiovascular disease. S100A7, A8/A9, and A12 are protein complexes that are produced by activated neutrophils, monocytes, and keratinocytes in psoriasis. Lipid-rich necrotic core (LRNC) is a high-risk coronary plaque feature previously found to be associated with cardiovascular risk factors and psoriasis severity.

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Background And Objectives: Psoriasis is a heterogeneous inflammatory disease that involves the skin, joints, liver, heart, and other organs. Psoriatic arthritis (PsA) is associated with cardiovascular disease (CVD), but the relative contributions of inflammatory and metabolic dysregulation to CVD are incompletely understood. We set out to discover novel potential contributors to CVD in PsA patients by comprehensively phenotyping a cohort of PsA patients using these advanced technologies.

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Article Synopsis
  • Traditional lipid measures and coronary imaging are helpful for assessing cardiovascular disease (CVD) risk, but more effective diagnostic tools are needed.
  • In a study of 795 people, those with low levels of apolipoprotein E-containing HDL-cholesterol (ApoE-HDL-C) showed worse coronary artery health, with more blockage and higher coronary artery calcium scores.
  • The findings suggest that low ApoE-HDL-C and high levels of apolipoprotein C-III (ApoC-III) could serve as significant indicators of CVD severity, highlighting their potential role in improving risk assessment.
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Background And Aims: Psoriasis is an immune-mediated inflammatory disease with increased risk of myocardial infarction. Preclinical studies in psoriasis models show an association between chronic inflammation and immune cell proliferation in the spleen and bone marrow (BM). We sought to test the hypothesis that splenic and BM F-fluorodeoxyglucose (F-FDG) uptake is heightened in psoriasis and that higher uptake associates with systemic inflammation and subclinical atherosclerotic disease measures in this cohort.

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The molecular mechanisms governing orderly shutdown and retraction of CD4 type 1 helper T (T1) cell responses remain poorly understood. Here we show that complement triggers contraction of T1 responses by inducing intrinsic expression of the vitamin D (VitD) receptor and the VitD-activating enzyme CYP27B1, permitting T cells to both activate and respond to VitD. VitD then initiated the transition from pro-inflammatory interferon-γ T1 cells to suppressive interleukin-10 cells.

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Article Synopsis
  • Increased left ventricular (LV) mass is linked to heart failure and is influenced by systemic inflammation; this study specifically looks at the role of subclinical coronary artery disease (CAD) in this relationship in individuals with psoriasis.
  • The research involved 189 psoriasis patients without known cardiovascular disease, measuring systemic inflammation via plasma glycoprotein A (GlycA) and LV mass using coronary CT angiography (CCTA); results showed a significant association between both GlycA and noncalcified coronary burden (NCB) with LV mass.
  • Findings indicate that systemic inflammation and early CAD (represented by NCB) contribute to increased LV mass independently from traditional cardiovascular risk factors, with about 32% of the GlycA-LV mass
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Article Synopsis
  • The study aimed to explore the link between abdominal subcutaneous adipose tissue (ASAT) and coronary atherosclerosis in people with psoriasis.
  • It involved 232 participants undergoing imaging tests to measure their fat tissue and assess heart disease risk, revealing different correlations between ASAT and inflammation or cholesterol levels based on sex.
  • Results showed that in men, higher ASAT was linked to lower coronary atherosclerosis risk, while no significant relationship was found for women, indicating the need for further research on how ASAT interacts with chronic inflammation in different sexes.
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Psoriasis is associated with a higher risk of liver diseases. We investigated the impact of hepatic steatosis (European cohort) and hepatic inflammation (United States cohort) on subclinical atherosclerosis. In the European cohort (n = 76 psoriasis participants and 76 controls), nonalcoholic fatty liver disease, assessed by the sonographic hepatorenal index, was more prevalent in psoriasis than in controls (61% vs.

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Psychosocial stress correlates with cardiovascular (CV) events; however, associations between physiologic measures of stressors and CVD remain incompletely understood, especially in racial/ethnic minority populations in resource-limited neighborhoods. We examined associations between chronic stress-related neural activity, measured by amygdalar Fluorodeoxyglucose (FDG) uptake, and aortic vascular FDG uptake (arterial inflammation measure) in a community-based cohort. Forty participants from the Washington, DC CV Health and Needs Assessment (DC-CHNA), a study of a predominantly African-American population in resource-limited urban areas and 25 healthy volunteers underwent detailed phenotyping, including FDG PET/CT for assessing amygdalar activity (AmygA), vascular FDG uptake, and hematopoietic (leukopoietic) tissue activity.

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Intermittent fasting blunts inflammation in asthma and rheumatoid arthritis, suggesting that fasting may be exploited as an immune-modulatory intervention. However, the mechanisms underpinning the anti-inflammatory effects of fasting are poorly characterized. Here, we show that fasting in humans is sufficient to blunt CD4 T helper cell responsiveness.

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Background: Inflammation in the form of elevated high-sensitivity c-reactive protein (hs-CRP) has been shown to be critical in the development of atherothrombosis. Psoriasis, a chronic inflammatory skin disease, is associated with high systemic-inflammation, elevated neutrophil-to-lymphocyte ratio (NLR) and accelerated non-calcified coronary artery burden (NCB) by coronary computed tomography angiography (CCTA). We hypothesized that NLR would associate with early, rupture-prone atherosclerosis assessed as NCB independent of hs-CRP.

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