Plasmacytoid dendritic cell content is associated with plasma aldosterone concentration in patients with primary aldosteronism.

Background: Inflammation plays a pivotal role in blood pressure regulation. Current data reflect the important role of T cells in primary hypertension. The role of dendritic cells (DC) in secondary hypertension- primary aldosteronism (PA) remains unknown.

A heart-brain-spleen axis controls cardiac remodeling to hypertensive stress.

Hypertensive heart disease (HTN-HD) meaningfully contributes to hypertension morbidity and mortality. Initially established as an adaptive response, HTN-HD progresses toward worsening of left ventricule (LV) function and heart failure (HF). Hypertensive stress elevates sympathetic nervous system (SNS) activity, a negative clinical predictor, and expands macrophages.

Novel Insight into Inflammatory Pathways in Acute Pulmonary Embolism in Humans.

Accumulating data have shown a pathophysiological association between inflammatory pathways and thrombosis. Venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and acute pulmonary embolism (APE), is a significant health burden. It involves not only hemodynamic disturbances due to the emboli occluding the pulmonary arteries, but also platelet activation, endothelial dysfunction, and "firing up" of the inflammatory cascade.

Vascular remodelling in cardiovascular diseases: hypertension, oxidation, and inflammation.

Optimal vascular structure and function are essential for maintaining the physiological functions of the cardiovascular system. Vascular remodelling involves changes in vessel structure, including its size, shape, cellular and molecular composition. These changes result from multiple risk factors and may be compensatory adaptations to sustain blood vessel function.

Sex-specific associations between the environmental exposures and low-grade inflammation and increased blood pressure in young, healthy subjects.

Long-term exposures to environmental factors including airborne as well as noise pollutants, are associated with cardiovascular risk. However, the influence of environmental pollution on the young population is controversial. Accordingly, we aimed to investigate the relationships between long-term exposures to different environmental factors and major cardiovascular and inflammatory parameters and biomarkers in young, healthy subjects.

Acute Pulmonary Embolism and Immunity in Animal Models.

Venous thromboembolism, encompassing acute pulmonary embolism (APE) and deep vein thrombosis (DVT), is a potentially fatal disease with complex pathophysiology. Traditionally, the Virchow triad provided a framework for understanding the pathogenic contributors to thrombus formation, which include endothelial dysfunction, alterations in blood flow and blood hypercoagulability. In the last years, it has become apparent that immunity plays a central role in thrombosis, interacting with classical prothrombotic mechanisms, oxidative stress and vascular factors.

Systemic and local vascular inflammation and arterial reactive oxygen species generation in patients with advanced cardiovascular diseases.

Background: Systemic inflammation may cause endothelial activation, mediate local inflammation, and accelerate progression of atherosclerosis. We examined whether the levels of circulating inflammatory cytokines reflect local vascular inflammation and oxidative stress in two types of human arteries.

Methods: Human internal mammary artery (IMA) was obtained in 69 patients undergoing coronary artery bypass graft (CABG) surgery and left anterior descending (LAD) artery was obtained in 17 patients undergoing heart transplantation (HTx).

Breast cancer chemotherapy induces vascular dysfunction and hypertension through a NOX4-dependent mechanism.

Cardiovascular disease is the major cause of morbidity and mortality in breast cancer survivors. Chemotherapy contributes to this risk. We aimed to define the mechanisms of long-term vascular dysfunction caused by neoadjuvant chemotherapy (NACT) and identify novel therapeutic targets.

Th17/Treg imbalance in patients with primary hyperaldosteronism and resistant hypertension.

Introduction: Inflammation plays a pivotal role in blood pressure regulation. Data on experimental models of hypertension and hypertensive patients reflect the imbalance between T regulatory (Treg) and Th17 effector cells (Th17).

Objectives: The aim of this study was to quantify peripheral blood Treg lymphocytes and Th17 subsets in individuals with primary hyperaldosteronism (PHA) and resistant hypertension (RHT) presenting with elevated blood pressure levels and augmented cardiovascular risk when compared with normotensive controls (CTRL).

Periodontitis as an inflammatory trigger in hypertension: From basic immunology to clinical implications.

Hypertension and periodontitis are both highly prevalent co-morbidities worldwide, and their occurrence increases with age. Multiple observational epidemiological studies have shown that periodontitis is associated with an increased cardiovascular disease (CVD) occurrence. Large systematic reviews and metanalyses further show that periodontitis increases the risk of hypertension and is associated with increased systolic and diastolic blood pressure.

Role of inflammatory chemokines in hypertension.

Hypertension is associated with immune cells activation and their migration into the kidney, vasculature, heart and brain. These inflammatory mechanisms are critical for blood pressure regulation and mediate target organ damage, creating unique novel targets for pharmacological modulation. In response to angiotensin II and other pro-hypertensive stimuli, the expression of several inflammatory chemokines and their receptors is increased in the target organs, mediating homing of immune cells.

Oleacein and Foam Cell Formation in Human Monocyte-Derived Macrophages: A Potential Strategy Against Early and Advanced Atherosclerotic Lesions.

Background: Oleacein is a secoiridoid group polyphenol found mostly in Olea europea L. and Ligustrum vulgare L. (Oleaceae).

Causal association between periodontitis and hypertension: evidence from Mendelian randomization and a randomized controlled trial of non-surgical periodontal therapy.

Aims: Inflammation is an important driver of hypertension. Periodontitis is a chronic inflammatory disease, which could provide a mechanism for pro-hypertensive immune activation, but evidence of a causal relationship in humans is scarce. We aimed to investigate the nature of the association between periodontitis and hypertension.

Adaptive Immunity in Hypertension.

Purpose Of Review: In recent years, a vast body of evidence has accumulated indicating the role of the immune system in the regulation of blood pressure and modulation of hypertensive pathology. Numerous cells of the immune system, both innate and adaptive immunity, have been indicated to play an important role in the development and maintenance of hypertension. The purpose of this review was to summarize the role of adaptive immunity in experimental models of hypertension (genetic, salt-sensitive, and Angiotensin (Ang) II induced) and in human studies.

1,2,3,4,6-Penta-O-galloyl-β-d-glucose modulates perivascular inflammation and prevents vascular dysfunction in angiotensin II-induced hypertension.

Background And Purpose: Hypertension is a multifactorial disease, manifested by vascular dysfunction, increased superoxide production, and perivascular inflammation. In this study, we have hypothesized that 1,2,3,4,6-penta-O-galloyl-β-d-glucose (PGG) would inhibit vascular inflammation and protect from vascular dysfunction in an experimental model of hypertension.

Experimental Approach: PGG was administered to mice every 2 days at a dose of 10 mg·kg i.

TNF-α Inhibitors Decrease Classical CD14CD16- Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis.

Monocytes are pivotal cells in inflammatory joint diseases. We aimed to determine the effect of TNF-α inhibitors (TNFi) on peripheral blood monocyte subpopulations and their activation in ankylosing spondylitis (AS) and rheumatoid arthritis (RA) patients with high disease activity. To address this, we studied 50 (32 AS, 18 RA) patients with highly active disease with no prior history of TNFi use who were recruited and assigned to TNFi or placebo treatment for 12 weeks.

Th1-type immune responses to Porphyromonas gingivalis antigens exacerbate angiotensin II-dependent hypertension and vascular dysfunction.

Background And Purpose: Emerging evidence indicates that hypertension is mediated by immune mechanisms. We hypothesized that exposure to Porphyromonas gingivalis antigens, commonly encountered in periodontal disease, can enhance immune activation in hypertension and exacerbate the elevation in BP, vascular inflammation and vascular dysfunction.

Experimental Approach: Th1 immune responses were elicited through immunizations using P.

Involvement of CD8+ T cell subsets in early response to vascular injury in patients with peripheral artery disease in vivo.

Aims: Adaptive immunity is critical in vascular remodelling following arterial injury. We hypothesized that acute changes in T cells at a percutaneous transluminal angioplasty (PTA) site could serve as an index of their potential interaction with the injured vascular wall.

Methods And Results: T cell subsets were characterised in 45 patients with Rutherford 3-4 peripheral artery disease (PAD) undergoing PTA.

Percutaneous Transluminal Angioplasty in Patients with Peripheral Arterial Disease Does Not Affect Circulating Monocyte Subpopulations.

Monocytes are mononuclear cells characterized by distinct morphology and expression of CD14 and CD16 surface receptors. Classical, quiescent monocytes are positive for CD14 (lipopolysaccharide receptor) but do not express Fc gamma receptor III (CD16). Intermediate monocytes coexpress CD16 and CD14.

Th responses are not altered by natural exposure to seasonal allergens in pollen-sensitive patients.

Background: Allergic rhinitis affects 10-30 % of the global population and this number is likely to increase in the forthcoming years. Moreover, it commonly co-exists with allergic asthma as a chronic allergic respiratory syndrome. While the involvement of Th cells in allergy is well understood, alterations of pro-inflammatory Th responses remain poorly characterized.