scholarly journals CRIP1 expression in monocytes related to hypertension

2021 ◽  
Author(s):  
Olga Schweigert ◽  
Julia Adler ◽  
Natalie Längst ◽  
Dylan Aïssi ◽  
Jorge Duque Escobar ◽  
...  
Keyword(s):  
Cohort Study ◽  
Immune System ◽  
Immune Cells ◽  
Genetic Factors ◽  
Endogenous Hormones ◽  
Ang Ii ◽  
Functional Link ◽  
Cysteine Rich Protein ◽  
Inflammatory Processes ◽  
Underlying Mechanisms

Hypertension is a complex and multifactorial disorder caused by lifestyle and environmental factors, inflammation and disease-related genetic factors and is a risk factor for stroke, ischemic heart disease and renal failure. Although circulating monocytes and tissue macrophages contribute to the pathogenesis of hypertension, the underlying mechanisms are poorly understood. Cysteine rich protein 1 (CRIP1) is highly expressed in immune cells, and CRIP1 mRNA expression in monocytes associates with blood pressure (BP) and is upregulated by proinflammatory modulation suggesting a link between CRIP1 and BP regulation through the immune system. To address this functional link, we studied CRIP1 expression in immune cells in relation to BP using a human cohort study and hypertensive mouse models. CRIP1 expression in splenic monocytes/macrophages and in circulating monocytes was significantly affected by angiotensin II (Ang II) in a BP-elevating dose (2 mg/kg/day). In the human cohort study, monocytic CRIP1 expression levels were associated with elevated BP, whereas upon differentiation of monocytes to macrophages this association along with the CRIP1 expression level was diminished. In conclusion, CRIP1-positive circulating and splenic monocytes seem to play an important role in hypertension related inflammatory processes through endogenous hormones such as Ang II. These findings suggest that CRIP1 may affect the interaction between the immune system, in particular monocytes, and the pathogenesis of hypertension.

Autoimmune diseases and gender gap

PNEI REVIEW ◽  
2020 ◽  
pp. 14-29
Author(s):  
Anna Giulia Bottaccioli ◽  
Francesco Bottaccioli
Keyword(s):  
Immune System ◽  
Social Relationships ◽  
Gender Gap ◽  
Immune Cells ◽  
Genetic Factors ◽  
External World ◽  
The Body ◽  
And Gender ◽  
The One ◽  
Microbial Agents

The concept of autoimmunity is both counterintuitive and anti-paradigmatic: indeed, during the last century, the immune system has been viewed as a defence system against external microbial agents - "the" cause of illness. However, the scientific research has found out that the immune system shows a much higher complexity, similarly to the nervous system: in particular, the immune system has an outstanding ability to adapt to the environment, which is defined by all the stimuli coming from either the inside of the body or the external world. Nutrition, physical activity, pollution, psychological stress, social relationships, and microbes (both symbiotic and pathogens) can greatly influence the activation of the immune system: on the one hand, the immune cells could be induced to orchestrate efficient responses to potential threats; on the other hand, they could be induced to attack the tissues of the body. The authors, therefore, aim to briefly review the research that showed how the environment, more than genetic factors, could influence the immune system, in particular, expanding on the reasons why autoimmunity appears to be way more prevalent in women than in men.

scholarly journals Elevated bone marrow sympathetic drive precedes systemic inflammation in angiotensin II hypertension

2019 ◽  
Vol 317 (2) ◽  
pp. H279-H289 ◽  
Author(s):  
Niousha Ahmari ◽  
Monica M. Santisteban ◽  
Douglas R. Miller ◽  
Natalie M. Geis ◽  
Riley Larkin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Bone Marrow ◽  
T Cells ◽  
Immune System ◽  
Angiotensin Ii ◽  
Paraventricular Nucleus ◽  
Immune Cells ◽  
Rodent Models ◽  
Ang Ii ◽  
Pressure Infiltration

Increased sympathetic nervous system activity is a hallmark of hypertension (HTN), and it is implicated in altered immune system responses in its pathophysiology. However, the precise mechanisms of neural-immune interaction in HTN remain elusive. We have previously shown an association between elevated sympathetic drive to the bone marrow (BM) and activated BM immune cells in rodent models of HTN. Moreover, microglial-dependent neuroinflammation is also seen in rodent models of HTN. However, the cause-effect relationship between central and systemic inflammatory responses and the sympathetic drive remains unknown. These observations led us to hypothesize that increase in the femoral BM sympathetic nerve activity (fSNA) initiates a cascade of events leading to increase in blood pressure (BP). Here, we investigated the temporal relationship between the BM sympathetic drive, activation of the central and peripheral immune system, and increase in BP in the events leading to established HTN. The present study demonstrates that central infusion of angiotensin II (ANG II) induces early microglial activation in the paraventricular nucleus of hypothalamus, which preceded increase in the fSNA. In turn, activation of fSNA correlated with the timing of increased production and release of CD4+.IL17+ T cells and other proinflammatory cells into circulation and elevation in BP, whereas infiltration of CD4+ cells to the paraventricular nucleus marked establishment of ANG II HTN. This study identifies cellular and molecular mechanisms involved in neural-immune interactions in early and established stages of rodent ANG II HTN. NEW & NOTEWORTHY Early microglia activation in paraventricular nucleus precedes sympathetic activation of the bone marrow. This leads to increased bone marrow immune cells and their release into circulation and an increase in blood pressure. Infiltration of CD4+ T cells into paraventricular nucleus paraventricular nucleus marks late hypertension.

scholarly journals Histopathology of the gut in rheumatic diseases

Reumatismo ◽  
2018 ◽  
pp. 178-186
Author(s):  
F. Macaluso ◽  
G. Guggino ◽  
A. Rizzo ◽  
A. Ferrante ◽  
F. Ciccia
Keyword(s):  
Immune System ◽  
Ankylosing Spondylitis ◽  
Rheumatic Diseases ◽  
Immune Cells ◽  
Genetic Factors ◽  
Intestinal Inflammation ◽  
Epithelial Barrier ◽  
Common Denominator ◽  
Intestinal Immune System ◽  
The Common

The gastrointestinal tract regulates the trafficking of macromolecules between the environment and the host through an epithelial barrier mechanism and is an important part of the immune system controlling the equilibrium between tolerance and immunity to non-self-antigens. Various evidence indicates that intestinal inflammation occurs in patients with rheumatic diseases. In many rheumatic diseases intestinal inflammation appears to be linked to dysbiosis and possibly represents the common denominator in the pathogenesis of different rheumatic diseases. The continuative interaction between dysbiosis and the intestinal immune system may lead to the aberrant activation of immune cells that can re-circulate from the gut to the sites of extraintestinal inflammation as observed in patients with ankylosing spondylitis. The exact contribution of genetic factors in the development of intestinal inflammation in rheumatic diseases needs to be clarified.

scholarly journals The immune system in hypertension

2014 ◽  
Vol 38 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Daniel W. Trott ◽  
David G. Harrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Immune Cells ◽  
Cell Activation ◽  
Immune Cell ◽  
Current Evidence ◽  
Interleukin 17 ◽  
Ang Ii ◽  
Immune Cell Activation

While hypertension has predominantly been attributed to perturbations of the vasculature, kidney, and central nervous system, research for almost 50 yr has shown that the immune system also contributes to this disease. Inflammatory cells accumulate in the kidneys and vasculature of humans and experimental animals with hypertension and likely contribute to end-organ damage. We and others have shown that mice lacking adaptive immune cells, including recombinase-activating gene-deficient mice and rats and mice with severe combined immunodeficiency have blunted hypertension to stimuli such as ANG II, high salt, and norepinephrine. Adoptive transfer of T cells restores the blood pressure response to these stimuli. Agonistic antibodies to the ANG II receptor, produced by B cells, contribute to hypertension in experimental models of preeclampsia. The central nervous system seems important in immune cell activation, because lesions in the anteroventral third ventricle block hypertension and T cell activation in response to ANG II. Likewise, genetic manipulation of reactive oxygen species in the subfornical organ modulates both hypertension and immune cell activation. Current evidence indicates that the production of cytokines, including tumor necrosis factor-α, interleukin-17, and interleukin-6, contribute to hypertension, likely via effects on both the kidney and vasculature. In addition, the innate immune system also appears to contribute to hypertension. We propose a working hypothesis linking the sympathetic nervous system, immune cells, production of cytokines, and, ultimately, vascular and renal dysfunction, leading to the augmentation of hypertension. Studies of immune cell activation will clearly be useful in understanding this common yet complex disease.

scholarly journals Aquaporins in Immune Cells and Inflammation: New Targets for Drug Development

2021 ◽  
Vol 22 (4) ◽  
pp. 1845
Author(s):  
Inês V. da Silva ◽  
Graça Soveral
Keyword(s):  
Hydrogen Peroxide ◽  
Immune System ◽  
Immune Cells ◽  
Volume Changes ◽  
Antigen Uptake ◽  
Inflammatory Conditions ◽  
Inflammatory Processes ◽  
Inflammation Resolution ◽  
Mammalian Immune System ◽  
Protein Channels

The mammalian immune system senses foreign antigens by mechanisms that involve the interplay of various kinds of immune cells, culminating in inflammation resolution and tissue clearance. The ability of the immune cells to communicate (via chemokines) and to shift shape for migration, phagocytosis or antigen uptake is mainly supported by critical proteins such as aquaporins (AQPs) that regulate water fluid homeostasis and volume changes. AQPs are protein channels that facilitate water and small uncharged molecules’ (such as glycerol or hydrogen peroxide) diffusion through membranes. A number of AQP isoforms were found upregulated in inflammatory conditions and are considered essential for the migration and survival of immune cells. The present review updates information on AQPs’ involvement in immunity and inflammatory processes, highlighting their role as crucial players and promising targets for drug discovery.

Virome and Inflammasomes, a Finely Tuned Balance with Important Consequences for the Host Health

2019 ◽  
Vol 26 (6) ◽  
pp. 1027-1044 ◽  
Author(s):  
Giulia Freer ◽  
Fabrizio Maggi ◽  
Mauro Pistello
Keyword(s):  
Immune System ◽  
Human Beings ◽  
Review Of The Literature ◽  
Adaptive Immune ◽  
Downstream Effects ◽  
Host Health ◽  
Inflammatory Processes ◽  
Human Immune ◽  
Immune Defences

Background:The virome is a network of viruses normally inhabiting humans. It forms a conspicuous portion of the so-called microbiome, once generically referred to as resident flora. Indeed, viruses infecting humans without leading to clinical disease are increasingly recognized as part of the microbiome and have an impact on the development of our immune system. In addition, they activate inflammasomes, multiprotein complexes that assemble in cells and that are responsible for the downstream effects of sensing pathogens.Objective:This review aims at summarizing the evidence on the role of the virome in modulating inflammation and emphasizes evidence for Anelloviruses as useful molecular markers to monitor inflammatory processes and immune system competence.Method:We carried out a review of the literature published in the last 5 years and summarized older literature to take into account ground-breaking discoveries concerning inflammasome assembly and virome.Results:A massive amount of data recently emerging demonstrate that the microbiome closely reflects what we eat, and many other unexpected variables. Composition, location, and amount of the microbiome have an impact on innate and adaptive immune defences. Viruses making up the virome contribute to shaping the immune system. Anelloviruses, the best known of such viruses, are present in most human beings, persistently without causing apparent disease. Depending on their interplay with such viruses, inflammasomes instruct host defences to tolerate or forfeit a specific microorganism.Conclusion:The virome plays an important role in shaping human immune defences and contributes to inflammatory processes by quenching or increasing them.

The Immune System Regulation in Sepsis: From Innate to Adaptive

2019 ◽  
Vol 20 (8) ◽  
pp. 799-816 ◽  
Author(s):  
Yue Qiu ◽  
Guo-wei Tu ◽  
Min-jie Ju ◽  
Cheng Yang ◽  
Zhe Luo
Keyword(s):  
Clinical Trials ◽  
Immune System ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Immune Cells ◽  
Current Knowledge ◽  
Systemic Inflammatory Response ◽  
Immune System Regulation

Sepsis, which is a highly heterogeneous syndrome, can result in death as a consequence of a systemic inflammatory response syndrome. The activation and regulation of the immune system play a key role in the initiation, development and prognosis of sepsis. Due to the different periods of sepsis when the objects investigated were incorporated, clinical trials often exhibit negative or even contrary results. Thus, in this review we aim to sort out the current knowledge in how immune cells play a role during sepsis.

Pathway of Inflammation due to Asbestiform fiber "Fluoro-edenite" Exposure: an Update

2020 ◽  
Vol 16 ◽  
Author(s):  
Caterina Ledda ◽  
Claudia Lombardo ◽  
Elisabetta A. Tendi ◽  
Maria Hagnas ◽  
Gianluca Paravizzini ◽  
...  
Keyword(s):  
Immune System ◽  
Autoimmune Disease ◽  
Early Response ◽  
The Body ◽  
Volcanic Area ◽  
Asbestos Fibers ◽  
Inflammatory Processes

: Fluoro-edenite (FE) is an asbestos-like amphibole present in the bentonitic lavas extracted from a stone quarry in Biancavilla, a village sited in the Etnean Volcanic Area (Italy). : Thoracic pathologies are the results of excessive inflammatory processes that are the early response of the immune system to inhaled fibers. As demonstrated for asbestos, fibers may trigger immune system cells in an acute and/or chronic manner. This review aims to clarify the pathways of inflammation in workers exposed to FE fibers. : Based on the articles reviewed, it seems that a permanent stimulus created by repeatedly inhaling the FE fibers and their persistence in the body can act as trigger both in promoting inflammatory processes and in immunological induction of autoimmune disease.

Platelets: Angels and demons dancing on the immune stage. Nutrition conducts the orchestra

2020 ◽  
Vol 20 ◽  
Author(s):  
Thea Magrone ◽  
Manrico Magrone ◽  
Matteo Antonio Russo ◽  
Emilio Jirillo
Keyword(s):  
Platelet Function ◽  
Immune Cells ◽  
Dual Role ◽  
Immune Functions ◽  
Omega 3 ◽  
Adaptive Immune ◽  
Cytokines And Chemokines ◽  
Adaptive Immune Cells ◽  
Immune Mediated ◽  
Inflammatory Processes

Background: Platelets are cellular fragments derived from bone-marrow megacaryocytes and they are mostly involved in haemostasis and coagulation. However, according to recent data, platelets are able to perform novel immune functions. In fact, they possess a receptorial armamentarium on their membrane for interacting with innate and adaptive immune cells. In addition, platelets also secrete granules which contain cytokines and chemokines for activating and recruiting even distant immune cells. Objectives: The participation of platelets in inflammatory processes will be discussed also in view of their dual role in terms of triggering or resolving inflammation. Involvement of platelets in disease will be illustrated, pointing to their versatile function to either up- or down-regulate pathological mechanisms. Finally, despite the availability of some anti-platelet agents, such as aspirin, dietary manipulation of platelet function is currently investigated. In this regard, special emphasis will be placed on dietary omega-3 polyunsaturated fatty acids (PUFAs) and polyphenol effects on platelets. Conclusion: Platelets play a dual role in inflammatory-immune-mediated diseases either activating or deactivating immune cells. Diet based on substances, such as omega-3 PUFAs and polyphenols, may act as a modulator of platelet function, even if more clinical trials are needed to corroborate such a contention.

scholarly journals POS1329 A COHORT STUDY ON THE RISK OF DEVELOPING OBSTRUCTIVE SLEEP APNEA, TEMPOROMANDIBULAR JOINT DISORDERS AND CRANIOFACIAL DEFORMITIES IN PATIENTS WITH JUVENILE IDIOPATHIC ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 947.1-947
Author(s):  
K. S. K. MA ◽  
L. T. Wang
Keyword(s):  
Obstructive Sleep Apnea ◽  
Cohort Study ◽  
Juvenile Idiopathic Arthritis ◽  
Cox Proportional Hazard Model ◽  
Proportional Hazard ◽  
Proportional Hazard Model ◽  
Cox Proportional Hazard ◽  
Obstructive Sleep ◽  
Subgroup Analyses ◽  
Underlying Mechanisms

Background:Juvenile Idiopathic Arthritis (JIA), an autoimmune disease, has been proposed to be comorbid with obstructive sleep apnea (OSA).Objectives:We aimed at identifying the relationship between JIA and OSA.Methods:We performed a cohort study including JIA and OSA patients from 1999 to 2013. A total of 2791 patients diagnosed with OSA after JIA onset were recruited, which 11,164 eligible individuals without JIA history were selected as matched-controls. A Cox proportional hazard model was developed to estimate the risk of OSA in JIA patients. A cumulative probability model was adopted to assess the time-dependent effect of JIA on OSA development, implying the casual link of the association. To identify whether JIA patients have higher risks for developing temporomandibular joint (TMJ) disorders, craniofacial anomalies and deformities than non-JIA individuals, subgroup analyses was conducted. Finally, Ingenuity Systems Pathway Analysis (IPA) was conducted to identify underlying mechanisms of the above disease correlation among peripheral blood mononuclear cells (PBMCs) from rheumatic factor (RF)-positive and RF-negative JIA patients, and subcutaneous fat tissues from OSA patients, using p-value visualization for RNA-seq analyses.Results:The Cox proportional hazard model showed that JIA patients were more likely to have OSA than non-JIA individuals (adjusted hazard ratio =1.949, 95% CI =1.264–3.005). The incidence of developing OSA was particularly high among patients who developed JIA aged 18-30 years old (aHR= 2.034, 95% CI=1.305-3.169) and males (aHR=1.82, 95% CI=1.121-2.954). The risk of developing OSA increased within 0-36 months (aHR = 2.216, 95% CI = 1.001 – 4.907) and over 60 months (aHR = 2.558, 95% CI = 1.346 – 4.860) of follow-up duration after JIA onset. Subgroup analyses showed that JIA patients were more likely to have TMJ disorders (relative risk = 2.047, 95% CI = 1.446-2.898) and to receive treatment for craniofacial deformities (RR = 1.722, 95% CI = 1.38-2.148) than non-JIA controls. IPA analyses suggested that the underlying mechanisms involved activation of antigen presentation pathway followed by antigen presentation to CD4+ and CD8+ T lymphocytes, as well as B cell development.Conclusion:Our findings identified high risks of developing OSA, TMJ disorders, and craniofacial deformities following JIA onset, which the underlying mechanisms may involve both cellular and humoral immunity.Disclosure of Interests:None declared

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