scholarly journals Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways

2006 ◽  
Vol 86 (2) ◽  
pp. 515-581 ◽  
Author(s):  
Alain Tedgui ◽  
Ziad Mallat
Keyword(s):  
Inflammatory Cytokines ◽  
Transforming Growth Factor ◽  
Current Knowledge ◽  
Thrombus Formation ◽  
Critical Role ◽  
Interleukin 10 ◽  
Vascular Events ◽  
Regulatory Pathways ◽  
Anti Inflammatory

Atherosclerosis is a chronic disease of the arterial wall where both innate and adaptive immunoinflammatory mechanisms are involved. Inflammation is central at all stages of atherosclerosis. It is implicated in the formation of early fatty streaks, when the endothelium is activated and expresses chemokines and adhesion molecules leading to monocyte/lymphocyte recruitment and infiltration into the subendothelium. It also acts at the onset of adverse clinical vascular events, when activated cells within the plaque secrete matrix proteases that degrade extracellular matrix proteins and weaken the fibrous cap, leading to rupture and thrombus formation. Cells involved in the atherosclerotic process secrete and are activated by soluble factors, known as cytokines. Important recent advances in the comprehension of the mechanisms of atherosclerosis provided evidence that the immunoinflammatory response in atherosclerosis is modulated by regulatory pathways, in which the two anti-inflammatory cytokines interleukin-10 and transforming growth factor-β play a critical role. The purpose of this review is to bring together the current information concerning the role of cytokines in the development, progression, and complications of atherosclerosis. Specific emphasis is placed on the contribution of pro- and anti-inflammatory cytokines to pathogenic (innate and adaptive) and regulatory immunity in the context of atherosclerosis. Based on our current knowledge of the role of cytokines in atherosclerosis, we propose some novel therapeutic strategies to combat this disease. In addition, we discuss the potential of circulating cytokine levels as biomarkers of coronary artery disease.

Traditional drink of black cincau (Mesona palustris BL)-based wedang uwuh as immunomodulator on alloxan-induced diabetic rats

2020 ◽  
Vol 50 (6) ◽  
pp. 1123-1133
Author(s):  
Tri Dewanti Widyaningsih ◽  
Astri Iga Siska ◽  
Roudlatul Fanani ◽  
Erryana Martati
Keyword(s):  
Inflammatory Cytokines ◽  
Transforming Growth Factor ◽  
Interleukin 10 ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Immunomodulatory Effect ◽  
Immunomodulatory Activity ◽  
Content Type ◽  
Anti Inflammatory ◽  
Red Ginger

Purpose This study aims to evaluate the immunomodulatory effect of traditional drink of black cincau-based wedang uwuh (WUB) on alloxan-induced diabetic rats. Design/methodology/approach WUB consists of dried herbs such as black cincau leaves (Mesona palustris BL), red ginger (Zingiber officinale Rosc), cloves (Syzgium aromaticum), sappan wood (Caesalpinia sappan Lin) and soursop leaves (Annona muricata). In this study, the rats were divided into five groups: normal control, diabetic control and three groups of WUB (WUB 13.5 mL/kg and WUB 27 mL/kg) or wedang uwuh commercial (WUC) treated diabetic groups. WUB or WUC was administered by gavage for three days after rats were confirmed diabetic induced by alloxan; these injections were continued for 28 days. At the end of the experiment, the spleen of rats was analyzed using flow cytometry. Data were analyzed by ANOVA followed by Tukey test using Minitab version 16.0. Findings This study showed that WUB significantly inhibited the expression of pro-inflammatory cytokines (interferon-Y [IFN-ɣ] and tumor necrosis factor-α [TNF-a]) and anti-inflammatory cytokines (interleukin 10 [IL-10] and transforming growth factor-β [TGF-ß]), and achieved a balance between pro-inflammatory and anti-inflammatory cytokines that were not significantly different from normal controls. WUB 27 was able to regulate the production of relative average cytokines IFN-ɣ (7.6 ± 3.5; p = 0.010), TNF-a (8.7 ± 2.4; p = 0.018), IL-10 (6.3 ± 2.4; p = 0.001) and TGF-ß (7.4 ± 2.1; p = 0.004) that was significantly different from diabetic control. This study’s results validate that the use of WUB can result in immunomodulatory activity in diabetic rats. Originality/value To the best of the authors’ knowledge, this is the first study on the immunomodulatory effect of WUB which is developed based on WUC; WUB has been used by Indonesian people as a functional beverage which acts as an immune booster and body warmer.

Harnessing the platelet

1997 ◽  
Vol 6 (5) ◽  
pp. 406-414 ◽  
Author(s):  
LG Futterman ◽  
L Lemberg
Keyword(s):  
Platelet Aggregation ◽  
Thrombus Formation ◽  
Critical Role ◽  
Vascular Events ◽  
New Class ◽  
Fibrinogen Receptor ◽  
Platelet Receptor ◽  
Thrombotic Complications ◽  
Coronary Events

Appreciation of the critical role of platelets in cardiovascular disease came when it was shown that aspirin, by virtue of its ability to block platelet aggregation, reduced the combined incidence of MI, stroke, and vascular death by 25%. Understanding the key role played by platelets in acute thrombotic vascular events prompted the development of a new class of drugs to control platelet action. Platelet aggregation is mediated exclusively by the platelet fibrinogen receptor GP IIb/IIIa. The binding of the receptor with fibrinogen is the final common pathway leading to platelet aggregation and thrombus formation. Abciximab, the first GP IIb/IIIa platelet receptor inhibitor, effectively reduces the thrombotic complications in acute coronary vascular events. The newer GP IIb/IIIa inhibitors, the synthetic peptide antagonists, have been shown to be more specific, to be nonimmunogenic, and to cause less bleeding. It is predictable that an oral GP IIb/IIIa inhibitor will become part of the standard repertoire in patients with unstable angina. The platelet has taken center stage in the battle against arterial thrombosis. The direction of our medical attack on acute coronary events is clear: harness the platelet.

scholarly journals Dual Role of Interleukin-10 in Murine NZB/W F1 Lupus

2021 ◽  
Vol 22 (3) ◽  
pp. 1347
Author(s):  
Anaïs Amend ◽  
Natalie Wickli ◽  
Anna-Lena Schäfer ◽  
Dalina T. L. Sprenger ◽  
Rudolf A. Manz ◽  
...  
Keyword(s):  
B Cell ◽  
Disease Model ◽  
Interleukin 10 ◽  
Immune Functions ◽  
Murine Lupus ◽  
Anti Inflammatory ◽  
In Vivo Effects

As a key anti-inflammatory cytokine, IL-10 is crucial in preventing inflammatory and autoimmune diseases. However, in human and murine lupus, its role remains controversial. Our aim was to understand regulation and immunologic effects of IL-10 on different immune functions in the setting of lupus. This was explored in lupus-prone NZB/W F1 mice in vitro and vivo to understand IL-10 effects on individual immune cells as well as in the complex in vivo setting. We found pleiotropic IL-10 expression that largely increased with progressing lupus, while IL-10 receptor (IL-10R) levels remained relatively stable. In vitro experiments revealed pro- and anti-inflammatory IL-10 effects. Particularly, IL-10 decreased pro-inflammatory cytokines and slowed B cell proliferation, thereby triggering plasma cell differentiation. The frequent co-expression of ICOS, IL-21 and cMAF suggests that IL-10-producing CD4 T cells are important B cell helpers in this context. In vitro and in vivo effects of IL-10 were not fully concordant. In vivo IL-10R blockade slightly accelerated clinical lupus manifestations and immune dysregulation. Altogether, our side-by-side in vitro and in vivo comparison of the influence of IL-10 on different aspects of immunity shows that IL-10 has dual effects. Our results further reveal that the overall outcome may depend on the interplay of different factors such as target cell, inflammatory and stimulatory microenvironment, disease model and state. A comprehensive understanding of such influences is important to exploit IL-10 as a therapeutic target.

scholarly journals Regulation of the Anti-Inflammatory Cytokines Interleukin-4 and Interleukin-10 during Pregnancy

2014 ◽  
Vol 5 ◽  
Author(s):  
Piyali Chatterjee ◽  
Valorie L. Chiasson ◽  
Kelsey R. Bounds ◽  
Brett M. Mitchell
Keyword(s):  
Inflammatory Cytokines ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Anti Inflammatory

scholarly journals CHEK2∗1100delC Mutation and Risk of Prostate Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Victoria Hale ◽  
Maren Weischer ◽  
Jong Y. Park
Keyword(s):  
Prostate Cancer ◽  
Current Knowledge ◽  
Prostate Cancer Screening ◽  
Critical Role ◽  
Prostate Cancer Risk ◽  
Conclusive Evidence ◽  
Increased Risk ◽  
History Of ◽  
Cancer Studies

Although the causes of prostate cancer are largely unknown, previous studies support the role of genetic factors in the development of prostate cancer.CHEK2plays a critical role in DNA replication by responding to double-stranded breaks. In this review, we provide an overview of the current knowledge of the role of a genetic variant, 1100delC, ofCHEK2on prostate cancer risk and discuss the implication for potential translation of this knowledge into clinical practice. Currently, twelve articles that discussedCHEK2∗1100delC and its association with prostate cancer were identified. Of the twelve prostate cancer studies, five studies had independent data to draw conclusive evidence from. The pooled results of OR and 95% CI were 1.98 (1.23–3.18) for unselected cases and 3.39 (1.78–6.47) for familial cases, indicating thatCHEK2∗1100delC mutation is associated with increased risk of prostate cancer. Screening for CHEK2∗1100delC should be considered in men with a familial history of prostate cancer.

scholarly journals Squalene Stimulates a Key Innate Immune Cell to Foster Wound Healing and Tissue Repair

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Cristina Sánchez-Quesada ◽  
Alicia López-Biedma ◽  
Estefania Toledo ◽  
José J. Gaforio
Keyword(s):  
Wound Healing ◽  
Inflammatory Cytokines ◽  
Tissue Repair ◽  
Immune Cell ◽  
Critical Role ◽  
Virgin Olive Oil ◽  
Skin Damage ◽  
Macrophage Response ◽  
Anti Inflammatory ◽  
Minor Compounds

Anti-inflammatory effects of virgin olive oil (VOO) have been described recently, along with its wound healing effect. One of the main minor compounds found in VOO is squalene (SQ), which also possesses preventive effects against skin damage and anti-inflammatory properties. The inflammatory response is involved in wound healing and manages the whole process by macrophages, among others, as the main innate cells with a critical role in the promotion and resolution of inflammation for tissue repair. Because of that, this work is claimed to describe the role that squalene exerts in the immunomodulation of M1 proinflammatory macrophages, which are the first cells implicate in recent injuries. Pro- and anti-inflammatory cytokines were analysed using TPH1 cell experimental model. SQ induced an increase in the synthesis of anti-inflammatory cytokines, such as IL-10, IL-13, and IL-4, and a decrease in proinflammatory signals, such as TNF-α and NF-κB in M1 proinflammatory macrophages. Furthermore, SQ enhanced remodelling and repairing signals (TIMP-2) and recruitment signals of eosinophils and neutrophils, responsible for phagocytosis processes. These results suggest that SQ is able to promote wound healing by driving macrophage response in inflammation. Therefore, squalene could be useful at the resolution stage of wound healing.

scholarly journals Anti-inflammatory role of curcumin in Lipopolysaccharide treated A549 cells at global proteome level and on mycobacterial infection

2019 ◽  
Author(s):  
Suchita Singh ◽  
Rakesh Arya ◽  
Rhishikesh R Bargaje ◽  
Mrinal Kumar Das ◽  
Subia Akram ◽  
...  
Keyword(s):  
Isotope Labeling ◽  
Small Cell Lung Carcinoma ◽  
Bacterial Load ◽  
Critical Role ◽  
A549 Cells ◽  
Molecular Evidence ◽  
Simultaneous Treatment ◽  
Cell Lung Carcinoma ◽  
Anti Inflammatory

AbstractA diet derived agent Curcumin (Diferuloylmethane), demonstrated its clinical application in inflammation, infection and cancer conditions. Nevertheless, its impact on the proteome of epithelial cells of non-small cell lung carcinoma (NSCLC) is yet to be explored. We employed a stable isotope labeling method for cell culture (SILAC) based relative quantitative proteomics and informatics analysis to comprehend global proteome change in A549 cells treated with curcumin and/or Lipopolysaccharide (LPS). Pretreated A549 cells were infected with Mycobacterium tuberculosis H37Rv strain to monitor bacterial load. With exposure to curcumin and LPS, out of the 1492 identified proteins, 305 and 346 proteins showed deregulation respectively. The expression of BID and AIFM1 mitochondrial proteins which play critical role in apoptotic pathway were deregulated in curcumin treated cells. Higher mitochondria intensity was observed in curcumin treated A549 cells than LPS treatment. Simultaneous treatment of curcumin and LPS neutralized the effect of LPS. Curcumin and/or LPS pretreated A549 cells infected with H37Rv, showed successful bacterial internalization. LPS treated A549 cells after infection showed increased bacterial load than curcumin compared to non-treated infected cells. However, simultaneous treatment of curcumin and LPS neutralized the effect of LPS. This study generated molecular evidence to deepen our understanding of the anti-inflammatory role of curcumin and may be useful to identify molecular targets for drug discovery.

scholarly journals Local and systemic influence of toxic levels of airborne ozone on the inflammatory response in rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Małgorzata Chmielewska-Krzesińska ◽  
Krzysztof Wąsowicz
Keyword(s):  
Inflammatory Response ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Genes Expression ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Necrosis Factor

Abstract Introduction Ozone is not harmful itself; however, it directly oxidises biomolecules and produces radical-dependent cytotoxicity. Exposure to ozone is by inhalation and therefore the lungs develop the main anti-inflammatory response, while ozone has an indirect impact on the other organs. This study investigated the local and systemic effects of the ozone-associated inflammatory response. Material and Methods Three groups each of 5 Wistar Han rats aged 6 months were exposed for 2h to airborne ozone at 0.5 ppm and a fourth identical group were unexposed controls. Sacrifice was at 3h after exposure for control rats and one experimental group and at 24 h and 48 h for the others. Lung and liver samples were evaluated for changes in expression of transforming growth factor beta 1, anti-inflammatory interleukin 10, pro-inflammatory tumour necrosis factor alpha and interleukin 1 beta and two nuclear factor kappa-light-chain-enhancer of B cells subunit genes. Total RNA was isolated from the samples in spin columns and cDNA was synthesised in an RT-PCR. Expression levels were compared to those of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and analysed statistically. Results All variables changed non-linearly over time comparing experimental groups to the control. Conspicuous expression changes in the subunit genes and cytokines were observed in both evaluated organs. Conclusion Locally and systemically, inflammation responses to ozone inhalation include regulation of certain genes’ expression. The mechanisms are unalike in lungs and liver but ozone exerts a similar effect in both organs. A broader range of variables influential on ozone response should be studied in the future.

scholarly journals Impact of Cigarette Smoking on Serum Pro- and Anti-Inflammatory Cytokines and Growth Factors

2015 ◽  
Vol 11 (4) ◽  
pp. 1169-1173 ◽  
Author(s):  
Mahdi Hasanzadeh Daloee ◽  
Amir Avan ◽  
Seyed Reza Mirhafez ◽  
Elahe Kavousi ◽  
Mehdi Hasanian-Mehr ◽  
...  
Keyword(s):  
Growth Factors ◽  
Cigarette Smoking ◽  
Inflammatory Cytokines ◽  
Female Group ◽  
Serum Concentrations ◽  
Medical Sciences ◽  
Cigarette Smokers ◽  
Tnf Α ◽  
Anti Inflammatory

Inflammation plays a key role in the initiation, progression, and clinical manifestation of atherosclerosis. Cigarette smoking is a risk factor for atherosclerosis and cardiovascular disease. The aim of the current study was to investigate the serum concentrations of 12 cytokines and growth factors (EGF, INF-γ, IL-1α/-1β/-2/-4/-6/-8/-10, MCP-1, TNF-α, and VEGF) in an Iranian population, including 192 smokers, comparing these values with concentrations in nonsmokers. One hundred and ninety-two cases were enrolled from the Mashhad University of Medical Sciences. Of these cases, 82 were cigarette smokers and 110 were nonsmokers. Sex and age were matched for the two groups. The serum concentration of 12 cytokines and growth factors were determined using EV-3513-cytokine-biochip arrays, by competitive chemiluminescence immunoassays. The level of serum MCP-1 was significantly ( p < .001) lower in the female group of cigarette smokers (mean = 88.1 dL/ng), compared with nonsmokers (mean = 155.6 dL/ng). There were no significant differences for the other cytokines and growth factors between the groups. Our finding demonstrate the association of MCP-1 with cigarette smoking, supporting further studies in larger population on evaluating the role of cigarette smoking on pro-/anti-inflammatory cytokines.

scholarly journals The role of the Th1 transcription factor T-bet in a mouse model of immune-mediated bone-marrow failure

Blood ◽  
2010 ◽  
Vol 115 (3) ◽  
pp. 541-548 ◽  
Author(s):  
Yong Tang ◽  
Marie J. Desierto ◽  
Jichun Chen ◽  
Neal S. Young
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Transcription Factor ◽  
Transforming Growth Factor ◽  
Bone Marrow Failure ◽  
Critical Role ◽  
Interferon Γ ◽  
Interleukin 17 ◽  
Immune Mediated

Abstract The transcription factor T-bet is a key regulator of type 1 immune responses. We examined the role of T-bet in an animal model of immune-mediated bone marrow (BM) failure using mice carrying a germline T-bet gene deletion (T-bet−/−). In comparison with normal C57BL6 (B6) control mice, T-bet−/− mice had normal cellular composition in lymphohematopoietic tissues, but T-bet−/− lymphocytes were functionally defective. Infusion of 5 × 106 T-bet−/− lymph node (LN) cells into sublethally irradiated, major histocompatibility complex–mismatched CByB6F1 (F1) recipients failed to induce the severe marrow hypoplasia and fatal pancytopenia that is produced by injection of similar numbers of B6 LN cells. Increasing T-bet−/− LN-cell dose to 10 to 23 × 106 per recipient led to only mild hematopoietic deficiency. Recipients of T-bet−/− LN cells had no expansion in T cells or interferon-γ–producing T cells but showed a significant increase in Lin−Sca1+CD117+CD34− BM cells. Plasma transforming growth factor-β and interleukin-17 concentrations were increased in T-bet−/− LN-cell recipients, possibly a compensatory up-regulation of the Th17 immune response. Continuous infusion of interferon-γ resulted in hematopoietic suppression but did not cause T-bet−/− LN-cell expansion or BM destruction. Our data provided fresh evidence demonstrating a critical role of T-bet in immune-mediated BM failure.

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