scholarly journals Role of placental inflammatory mediators and growth factors in patients with rheumatic diseases with a focus on systemic sclerosis

Rheumatology ◽  
2020 ◽  
Author(s):  
Francesca Motta ◽  
Veronica Codullo ◽  
Véronique Ramoni ◽  
Stefania Cesari ◽  
Giuseppina Ferrario ◽  
...  
Keyword(s):  
Growth Factors ◽  
Rheumatic Diseases ◽  
Inflammatory Mediators ◽  
Inflammatory Cells ◽  
Obstetric Complications ◽  
Histopathological Analysis ◽  
Increased Risk ◽  
Leucocyte Infiltration ◽  
Hepatocyte Growth

Abstract Objectives Pregnancy in SSc is burdened with an increased risk of obstetric complications. Little is known about the underlying placental alterations. This study aimed to better understand pathological changes and the role of inflammation in SSc placentas. Leucocyte infiltration, inflammatory mediators and atypical chemokine receptor 2 (ACKR2) expression in SSc placentas were compared with those in other rheumatic diseases (ORD) and healthy controls (HC). Methods A case–control study was conducted on eight pregnant SSc patients compared with 16 patients with ORD and 16 HC matched for gestational age. Clinical data were collected. Placentas were obtained for histopathological analysis and immunohistochemistry (CD3, CD20, CD11c, CD68, ACKR2). Samples from four SSc, eight ORD and eight HC were analysed by qPCR for ACKR2 expression and by multiplex assay for cytokines, chemokines and growth factors involved in angiogenesis and inflammation. Results The number of placental CD3, CD68 and CD11 cells was significantly higher in patients affected by rheumatic diseases (SSc+ORD) compared with HC. Hepatocyte growth factor was significantly increased in the group of rheumatic diseases patients (SSc+ORD) compared with HC, while chemokine (C-C motif) ligand 5 (CCL5) was significantly higher in SSc patients compared with ORD and HC. CCL5 levels directly correlated with the number of all local inflammatory cells and higher levels were associated with histological villitis. Conclusions Inflammatory alterations characterize placentas from rheumatic disease patients and could predispose to obstetric complications in these subjects.

scholarly journals The Role of Cytokines, Chemokines, and Growth Factors in the Pathogenesis of Pityriasis Rosea

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Francesco Drago ◽  
Giulia Ciccarese ◽  
Francesco Broccolo ◽  
Massimo Ghio ◽  
Paola Contini ◽  
...  
Keyword(s):  
Growth Factors ◽  
Human Herpesvirus ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Vascular Endothelial ◽  
Healthy Controls ◽  
Pityriasis Rosea ◽  
Vasculogenesis And Angiogenesis ◽  
Endothelial Growth Factor

Introduction. Pityriasis rosea (PR) is an exanthematous disease related to human herpesvirus- (HHV-) 6/7 reactivation. The network of mediators involved in recruiting the infiltrating inflammatory cells has never been studied.Object. To investigate the levels of serum cytokines, growth factors, and chemokines in PR and healthy controls in order to elucidate the PR pathogenesis.Materials and Methods. Interleukin- (IL-) 1, IL-6, IL-17, interferon- (IFN-)γ, tumor necrosis factor- (TNF-)α, vascular endothelial growth factor (VEGF), granulocyte colony stimulating factor (G-CSF), and chemokines, CXCL8 (IL-8) and CXCL10 (IP-10), were measured simultaneously by a multiplex assay in early acute PR patients’ sera and healthy controls. Subsequently, sera from PR patients were analysed at 3 different times (0, 15, and 30 days).Results and discussion. Serum levels of IL-17, IFN-γ, VEGF, and IP-10 resulted to be upregulated in PR patients compared to controls. IL-17 has a key role in host defense against pathogens stimulating the release of proinflammatory cytokines/chemokines. IFN-γhas a direct antiviral activity promoting NK cells and virus specific T cells cytotoxicity. VEGF stimulates vasculogenesis and angiogenesis. IP-10 can induce chemotaxis, apoptosis, cell growth, and angiogenesis.Conclusions. Our findings suggest that these inflammatory mediators may modulate PR pathogenesis in synergistic manner.

scholarly journals Autoantibodies and the Risk of Cardiovascular Events

2009 ◽  
Vol 36 (11) ◽  
pp. 2462-2469 ◽  
Author(s):  
KIMBERLY P. LIANG ◽  
HILAL MARADIT-KREMERS ◽  
CYNTHIA S. CROWSON ◽  
MELISSA R. SNYDER ◽  
TERRY M. THERNEAU ◽  
...  
Keyword(s):  
Rheumatic Diseases ◽  
Population Based ◽  
Cox Models ◽  
Diagnostic Indices ◽  
Increased Risk ◽  
Peptide Antibody ◽  
Cv Disease ◽  
Citrullinated Peptide ◽  
Overall Mortality

Objective.Inflammation and autoimmunity are associated with increased cardiovascular (CV) risk in patients with rheumatoid arthritis. This association may also be present in those without rheumatic diseases. Our purpose was to determine whether rheumatoid factor (RF), antinuclear antibody (ANA), and cyclic citrullinated peptide antibody (CCP) positivity are associated with increased risk of CV events and overall mortality in those with and without rheumatic diseases.Methods.We performed a population-based cohort study of all subjects who had a RF and/or ANA test performed between January 1, 1990, and January 1, 2000, and/or CCP test performed between September 1, 2003, and January 1, 2005, with followup until April 1, 2007. Outcomes were ascertained using diagnostic indices from complete medical records, including CV events [myocardial infarction (MI), heart failure (HF), and peripheral vascular disease (PVD)] and mortality. Cox models were used to analyze the data.Results.There were 6783 subjects with RF, 7852 with ANA, and 299 with CCP testing. Of these, 10.4%, 23.9%, and 14.7% were positive for RF, ANA, and CCP, respectively. Adjusting for age, sex, calendar year, comorbidity, and rheumatic disease, RF and ANA positivity were significant predictors of CV events [hazard ratio (HR) 1.24 and 1.26] and death (HR 1.43 and 1.18). Adjusting for age, CCP positivity was associated with CV events, but this association was not statistically significant (HR 3.1; 95% CI 0.8, 12.3).Conclusion.RF and ANA positivity are significant predictors of CV events and mortality in both those with and those without rheumatic diseases. These results support the role of immune dysregulation in the etiology of CV disease.

scholarly journals Role of Mouse Cytochrome P450 Enzymes of the Cyp2abfgs Subfamilies in the Induction of Lung Inflammation by Cigarette Smoke Exposure

2019 ◽  
Vol 172 (1) ◽  
pp. 123-131
Author(s):  
Matthew Hartog ◽  
Qing-Yu Zhang ◽  
Xinxin Ding
Keyword(s):  
Cytochrome P450 ◽  
Tobacco Smoke ◽  
Lung Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Cigarette Smoke Exposure ◽  
Histopathological Analysis ◽  
Cytochrome P450 Enzymes

Abstract Many constituents of tobacco smoke (TS) require bioactivation to exert toxic effects; however, few studies have examined the role of bioactivation enzymes in the adverse effects of TS exposure. This knowledge gap is a major source of uncertainty for risk assessment and chemoprevention efforts. Our aim is to test the hypothesis that cytochrome P450 (P450) enzyme-mediated bioactivation is essential to the development of TS exposure-induced lung toxicity, by determining the contributions of P450 enzymes in the mouse Cyp2abfgs gene subfamilies to environmental tobacco smoke (ETS)-induced lung inflammation. Adult female wildtype (WT) and Cyp2abfgs-null mice (both on C57BL/6J background) were exposed to filtered air or ETS, intermittently, for 1 or 2 weeks. Lung inflammation was assessed by quantification of inflammatory cells, cytokines, chemokines, and proteins in bronchoalveolar lavage fluid (BALF) and histopathological analysis. Glutathione (GSH) conjugates of 2 ETS constituents, naphthalene (NA), and 3-methylindole (3MI), were measured in mice exposed to ETS for 4 h. Persistent macrophagic and neutrophilic lung inflammation was observed in ETS-exposed WT mice; the extent of which was significantly reduced in ETS-exposed Cyp2abfgs-null mice. Levels of proinflammatory cytokines and chemokines, along with the total protein concentration, were increased in cell-free BALF from ETS-exposed WT mice, but not Cyp2abfgs-null mice. Additionally, GSH conjugates of NA and 3MI were detected in the lungs of WT, but not Cyp2abfgs-null, mice following ETS exposure. These results provide the first in vivo evidence that the mouse Cyp2abfgs gene cluster plays an important role in ETS-induced lung inflammation.

scholarly journals The Role of Osteoimmunology in Periodontal Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Rayyan A. Kayal
Keyword(s):  
Periodontal Disease ◽  
Inflammatory Mediators ◽  
Pathological Condition ◽  
Inflammatory Cells ◽  
Innate And Adaptive Immunity ◽  
Tooth Structure ◽  
Continuous State ◽  
Host Defense System ◽  
Bacterial Plaque

Periodontal disease is a pathological condition that involves inflammation of the tooth supporting structures. It occurs in response to the presence of bacterial plaque on the tooth structure. The host defense system, including innate and adaptive immunity, is responsible for combating the pathologic bacteria invading the periodontal tissue. Failure to eradicate the invading pathogens will result in a continuous state of inflammation where inflammatory cells such as lymphocytes, PMNs, and macrophages will continue to produce inflammatory mediators in an effort to destroy the invaders. Unfortunately, these inflammatory mediators have a deleterious effect on the host tissue as well as foreign microbes. One of the effects of these mediators on the host is the induction of matrix degradation and bone resorption through activation of proteases and other inflammatory mediators that activate osteoclasts.

scholarly journals Role of Adipokines in Atherosclerosis: Interferences with Cardiovascular Complications in Rheumatic Diseases

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Morena Scotece ◽  
Javier Conde ◽  
Rodolfo Gómez ◽  
Verónica López ◽  
Jesús Pino ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Cardiovascular Diseases ◽  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Cardiovascular Complications ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Pathologic Alteration ◽  
Holistic Vision

Patients with rheumatic diseases have an increased risk of mortality by cardiovascular events. In fact, several rheumatic diseases such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, and ankylosing spondylitis are associated with a higher prevalence of cardiovascular diseases (CVDs). Although traditional cardiovascular risk factors have been involved in the pathogenesis of cardiovascular diseases in rheumatic patients, these alterations do not completely explain the enhanced cardiovascular risk in this population. Obesity and its pathologic alteration of fat mass and dysfunction, due to an altered pattern of secretion of proinflammatory adipokines, could be one of the links between cardiovascular and rheumatic diseases. Indeed, the incidence of CVDs is augmented in obese individuals with rheumatic disorders. Thus, in this paper we explore in detail the relationships among adipokines, rheumatic diseases, and cardiovascular complications by giving to the reader a holistic vision and several suggestions for future perspectives and potential clinical implications.

scholarly journals Histopathological Studies on Virulence of Dipeptidyl Aminopeptidase IV (DPPIV) of Porphyromonasgingivalis in a Mouse Abscess Model: Use of a DPPIV-Deficient Mutant

2001 ◽  
Vol 69 (11) ◽  
pp. 7159-7161 ◽  
Author(s):  
Hisao Yagishita ◽  
Yumi Kumagai ◽  
Kiyoshi Konishi ◽  
Yukihiro Takahashi ◽  
Takaaki Aoba ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Type Strain ◽  
Wild Type Strain ◽  
Inflammatory Cells ◽  
Histopathological Analysis ◽  
Deficient Mutant ◽  
Wild Type ◽  
Dipeptidyl Aminopeptidase ◽  
Histopathological Studies

ABSTRACT To elucidate the role of dipeptidyl aminopeptidase IV (DPPIV) in the virulence of Porphyromonas gingivalis, mice were infected with either a wild-type strain or a DPPIV-deficient mutant using an abscess model. Histopathological analysis of the resulting lesions indicated that DPPIV participates in virulence through the destruction of connective tissue and the less effective mobilization of inflammatory cells.

scholarly journals The Adipokine Network in Rheumatic Joint Diseases

2019 ◽  
Vol 20 (17) ◽  
pp. 4091 ◽  
Author(s):  
Mar Carrión ◽  
Klaus W. Frommer ◽  
Selene Pérez-García ◽  
Ulf Müller-Ladner ◽  
Rosa P. Gomariz ◽  
...  
Keyword(s):  
Rheumatic Diseases ◽  
Inflammatory Responses ◽  
Functional Limitations ◽  
Inflammatory Cells ◽  
Signal Molecules ◽  
Lipocalin 2 ◽  
Effector Cells ◽  
Bidirectional Communication ◽  
Rheumatic Conditions

Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.

scholarly journals IL-33 in Rheumatic Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Yuanji Dong ◽  
Jixin Zhong ◽  
Lingli Dong
Keyword(s):  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Nk Cell ◽  
Killer Cell ◽  
Inflammatory Cells ◽  
Protective Role ◽  
Cell Group ◽  
Cancer Tissue ◽  
Interleukin 33

Interleukin-33 (IL-33) is a nuclear factor mainly expressed in barrier epithelium, endothelial cells, and fibroblast reticular cells. Some inflammatory cells also express IL-33 under certain conditions. The important role of IL-33 in allergic reactions, helminth infection, cancer, tissue fibrosis, chronic inflammation, organ transplantation, and rheumatic immune diseases has been extensively studied in recent years. IL-33 primarily activates various circulating and tissue-resident immune cells, including mast cell, group 2 innate lymphoid cell (ILC2), regulatory T cell (Treg), T helper 2 cell (Th2), natural killer cell (NK cell), and macrophage. Therefore, IL-33 plays an immunomodulatory role and shows pleiotropic activity in different immune microenvironments. The IL-33/serum stimulation-2 (ST2) axis has been shown to have a detrimental effect on rheumatoid arthritis, systemic lupus erythematosus, and other rheumatic diseases. Interestingly, IL-33 also plays a protective role in the repair of barrier epithelium and the activation of Tregs. Therefore, the role of IL-33/ST2 depends on the underlying pathological conditions in rheumatic diseases. This review focuses on the dual role of the IL-33/ST2 axis in rheumatic diseases.

Signalling by HGF/SF and Met: the role of heparan sulphate co-receptors

2006 ◽  
Vol 34 (3) ◽  
pp. 414-417 ◽  
Author(s):  
L.E. Kemp ◽  
B. Mulloy ◽  
E. Gherardi
Keyword(s):  
Growth Factors ◽  
Tissue Regeneration ◽  
Receptor Tyrosine Kinase ◽  
Heparan Sulphate ◽  
Signalling Pathways ◽  
Angiogenic Growth Factors ◽  
Scatter Factor ◽  
Hepatocyte Growth ◽  
Made In

The receptor tyrosine kinase Met and its ligand HGF/SF (hepatocyte growth factor/scatter factor) are essential in the signalling pathways required for embryogenesis and tissue regeneration. Aberrant signalling of this complex is also a feature of many tumours and appears to contribute to the growth, invasiveness and metastasis of both carcinomas and sarcomas. HGF/SF, like many other angiogenic growth factors, employs heparan sulphate as co-receptor. The role of this interaction has not been completely defined but appears to be physiologically relevant. Thus the presence of heparin increases the potency of HGF/SF in experiments with cells in culture leading to elevated downstream signalling effects and, although not vital for the Met–HGF/SF interaction, heparin or heparan sulphate is essential for the activity of certain isoforms of HGF/SF, such as NK1 and NK2. Here, we summarize the progress made in understanding the interaction between heparin and heparan sulphate and NK1, NK2 and HGF/SF and we discuss their role in HGF/SF–Met signalling.

Role of phytochemicals in the inhibition of epithelial–mesenchymal transition in cancer metastasis

2016 ◽  
Vol 7 (9) ◽  
pp. 3677-3685 ◽  
Author(s):  
Eun-Kyung Kim ◽  
Eun-Ju Choi ◽  
Trishna Debnath
Keyword(s):  
Growth Factors ◽  
Signaling Pathways ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Fibroblast Growth Factors ◽  
Fibroblast Growth ◽  
Scatter Factor ◽  
Mesenchymal Transition ◽  
Hepatocyte Growth

Epithelial–mesenchymal transition (EMT) development is controlled by several signaling pathways including Hedgehog, Wnt, fibroblast growth factors (FGF), hepatocyte growth factor/scatter factor (HGF),etc. Phytochemicals is very promising therapeutic candidate that inhibit the progression of EMT by inhibiting the signaling pathways.

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