scholarly journals Traditional Chinese Medicine Protects against Cytokine Production as the Potential Immunosuppressive Agents in Atherosclerosis

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yan Ren ◽  
Wei Qiao ◽  
Dongliang Fu ◽  
Zhiwei Han ◽  
Wei Liu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Therapeutic Strategy ◽  
Immunosuppressive Agents ◽  
Critical Factor ◽  
Chronic Inflammatory Disease ◽  
Atherosclerosis Progression ◽  
Adaptive Immune ◽  
Chinese Medicinal Plants ◽  
Anti Inflammatory ◽  
Accelerate Atherosclerosis

Atherosclerosis is a chronic inflammatory disease caused by dyslipidemia and mediated by both innate and adaptive immune responses. Inflammation is a critical factor at all stages of atherosclerosis progression. Proinflammatory cytokines accelerate atherosclerosis progression, while anti-inflammatory cytokines ameliorate the disease. Accordingly, strategies to inhibit immune activation and impede immune responses towards anti-inflammatory activity are an alternative therapeutic strategy to conventional chemotherapy on cardiocerebrovascular outcomes. Since a number of Chinese medicinal plants have been used traditionally to prevent and treat atherosclerosis, it is reasonable to assume that the plants used for such disease may suppress the immune responses and the resultant inflammation. This review focuses on plants that have immunomodulatory effects on the production of inflammatory cytokine burst and are used in Chinese traditional medicine for the prevention and therapy of atherosclerosis.

scholarly journals Immunobiology of Atherosclerosis: A Complex Net of Interactions

2019 ◽  
Vol 20 (21) ◽  
pp. 5293 ◽  
Author(s):  
Herrero-Fernandez ◽  
Gomez-Bris ◽  
Somovilla-Crespo ◽  
Gonzalez-Granado
Keyword(s):  
Immune Responses ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Atherosclerotic Lesion ◽  
Chronic Inflammatory Disease ◽  
Principal Factor ◽  
Global Perspective ◽  
Innate And Adaptive Immunity ◽  
Adaptive Immune ◽  
Apoptosis And Necrosis

Cardiovascular disease is the leading cause of mortality worldwide, and atherosclerosis the principal factor underlying cardiovascular events. Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction, intimal lipid deposition, smooth muscle cell proliferation, cell apoptosis and necrosis, and local and systemic inflammation, involving key contributions to from innate and adaptive immunity. The balance between proatherogenic inflammatory and atheroprotective anti-inflammatory responses is modulated by a complex network of interactions among vascular components and immune cells, including monocytes, macrophages, dendritic cells, and T, B, and foam cells; these interactions modulate the further progression and stability of the atherosclerotic lesion. In this review, we take a global perspective on existing knowledge about the pathogenesis of immune responses in the atherosclerotic microenvironment and the interplay between the major innate and adaptive immune factors in atherosclerosis. Studies such as this are the basis for the development of new therapies against atherosclerosis

scholarly journals Immune profiling demonstrates a common immune signature of delayed acquired immunodeficiency in patients with various etiologies of severe injury

2021 ◽  
Author(s):  
Fabienne Venet ◽  
Julien Textoris ◽  
Sophie Blein ◽  
Mary-Luz Rol ◽  
Maxime Bodinier ◽  
...  
Keyword(s):  
Immune Responses ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Secondary Infections ◽  
Increased Risk ◽  
Acquired Immunodeficiency ◽  
Anti Inflammatory ◽  
Immune Profiling

AbstractBackground and Research QuestionThe host response plays a central role in the pathophysiology of sepsis and severe injuries. So far, no study has comprehensively described the overtime changes of the injury-induced immune profile in a large cohort of critically ill patients with different etiologies.Study Design and Methods353 septic, trauma and surgical patients and 175 healthy volunteers were prospectively included in the REAnimation Low Immune Status Marker (REALISM) study. Extensive immune profiling was performed by assessing cellular phenotypes and functions, protein and mRNA levels at days 1-2, 3-4 and 5-7 after inclusion using a panel of 30 standardized immune markers.ResultsUsing REALISM immunomonitoring panel, no specificity in the immune profile was observed between septic, trauma and surgical patients. This common injury-induced immune response was characterized by an initial adaptive (i.e. physiologic) response engaging all constituents of the immune system (pro- and anti-inflammatory cytokine release, innate and adaptive immune responses) but not associated with increased risk of secondary infections. In contrary, the persistence in a subgroup of patients of profound immune alterations at the end of the first week after admission was associated with increased risk of secondary infections independently of exposure to invasive devices. The combined monitoring of markers of pro/anti-inflammatory, innate and adaptive immune responses allowed a better enrichment of patients with risk of secondary infections in the selected population.InterpretationThese results illustrate the delayed development of a common maladaptive injury-acquired immunodeficiency in a subgroup of severely injured patients independently of initial etiologies. Critically ill patients’ immune status could be captured through the combined monitoring a common panel of complementary markers of pro/anti-inflammatory, innate and adaptive immune responses. Such immune monitoring panel will help clinicians to identify critically ill patients who could benefit from tailored immunoadjuvant therapies.Clinical Trial Registrationclinicaltrials.gov: NCT02638779Summary conflict of interest statementsJT, SB, VM and AP are employees of bioMérieux SA, an in vitro diagnostic company. FV, TR, YB, BD, OM, TG, CT and GM are employees of Hospices Civils de Lyon. JT, TR, SB, VM, AP, FV and GM work in a joint research unit, co funded by the Hospices Civils de Lyon and bioMérieux. JT, AP, GM and FV are co-inventors in patent applications covering the following markers: CX3CR1, CD127, IL10 and S100A9. LKT and CT are employees of and hold stock and shares in GlaxoSmithKline. LQU is an employee of Sanofi Pasteur. PC was employee of Sanofi, Inc. and declares no other competing interests.Funding informationThis study received funding from the Agence Nationale de la Recherche through a grant awarded to BIOASTER (Grant number #ANR-10-AIRT-03) and from bioMérieux, Sanofi and GSK.

scholarly journals Anti-Inflammatory Therapies for Treatment of Inflammation-Related Preterm Brain Injury

2021 ◽  
Vol 22 (8) ◽  
pp. 4008
Author(s):  
Jaya D. Prasad ◽  
Katherine C. Gunn ◽  
Joanne O. Davidson ◽  
Robert Galinsky ◽  
Scott E. Graham ◽  
...  
Keyword(s):  
Brain Injury ◽  
Immune Responses ◽  
Therapeutic Strategy ◽  
Brain Cell ◽  
Neonatal Immunity ◽  
Neuroprotective Strategies ◽  
Infection And Inflammation ◽  
Anti Inflammatory ◽  
Neurobehavioral Deficits ◽  
Nonspecific Inflammation

Despite the prevalence of preterm brain injury, there are no established neuroprotective strategies to prevent or alleviate mild-to-moderate inflammation-related brain injury. Perinatal infection and inflammation have been shown to trigger acute neuroinflammation, including proinflammatory cytokine release and gliosis, which are associated with acute and chronic disturbances in brain cell survival and maturation. These findings suggest the hypothesis that the inhibition of peripheral immune responses following infection or nonspecific inflammation may be a therapeutic strategy to reduce the associated brain injury and neurobehavioral deficits. This review provides an overview of the neonatal immunity, neuroinflammation, and mechanisms of inflammation-related brain injury in preterm infants and explores the safety and efficacy of anti-inflammatory agents as potentially neurotherapeutics.

Abstract 586: CD40L on T Cells is a Major Contributor to Atherosclerosis in Hyperlipidemic Mice

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Norbert Gerdes ◽  
Christina Buerger ◽  
Holger Winkels ◽  
Christian Weber ◽  
Esther Lutgens
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Chronic Inflammatory Disease ◽  
Chow Diet ◽  
Gene Markers ◽  
Anti Inflammatory

Atherosclerosis is a lipid driven chronic inflammatory disease of the arterial wall, involving both innate and adaptive immune responses. Specialized immune cells such as monocytes, B cells, T cells and dendritic cells (DCs) contribute to disease progression or control the inflammatory responses. The CD40-CD40L dyad was identified as an efficient modulator of cellular immune responses. CD40 is a member of the tumor necrosis factor receptor (TNFR) superfamily and is activated by CD40 ligand (CD40L). CD40 and CD40L both are expressed on the majority of immune and non-immune cells associated with atherosclerosis. However, the specific contribution of CD40-CD40L signaling on the different single cell types towards atherosclerosis progression remains undefined. Here, we aimed to investigate the cell type-specific mechanisms of CD40-CD40L interactions in atherosclerosis by generating mice with a conditional ablation of CD40L on T cells. Hyperlipidemic mice with a T cell-specific deficiency of CD40L developed significantly smaller atherosclerotic lesions in the ascending after 28 weeks of chow diet, and following 6 weeks of a cholesterol-enriched diet when compared to their littermate controls. Changes in lesion size were accompanied by a modified anti-inflammatory plaque phenotype, characterized by an increased proportion of smooth muscle cells and a reduced number of pro-inflammatory immune cells, such as macrophages and T cells. T cell CD40L-deficient mice displayed systematically reduced expression of pro-inflammatory cytokines such as IL-1β, IL-2, IL-12, and IFNγ, and increased expression of anti-inflammatory cytokines IL-10 and TGFβ. This anti-inflammatory milieu was paralleled a change in the development and activation status of the T cells with mice lacking CD40L on T cells displaying a reduction in the expression of cytokines and gene markers associated with the activation of T cells (e.g., IL-2, CD69). This change was also reflected within the T cell populations which had a reduced proportion of activated effector T cells and an increased ratio of naïve T cells. Thus, our study ascribes CD40L on T cells a central role in atherosclerosis.

scholarly journals Antibodies against apoB100 peptide 210 inhibit atherosclerosis in apoE-/- mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Pontus Dunér ◽  
Ingrid Yao Mattisson ◽  
Per Fogelstrand ◽  
Lars Glise ◽  
Stacey Ruiz ◽  
...  
Keyword(s):  
Immune Responses ◽  
Antibody Response ◽  
Therapeutic Strategy ◽  
Atherosclerotic Plaques ◽  
Control Groups ◽  
Similar Reduction ◽  
Adaptive Immune ◽  
Atherosclerotic Plaque Formation ◽  
Severe Atherosclerosis

AbstractAtherosclerotic plaques are characterized by an accumulation and subsequent oxidation of LDL, resulting in adaptive immune responses against formed or exposed neoepitopes of the LDL particle. Autoantibodies against native p210, the 3136–3155 amino acid sequence of the LDL protein apolipoprotein B-100 (apoB100) are common in humans and have been associated with less severe atherosclerosis and decreased risk for cardiovascular events in clinical studies. However, whether apoB100 native p210 autoantibodies play a functional role in atherosclerosis is not known. In the present study we immunized apoE-/- mice with p210-PADRE peptide to induce an antibody response against native p210. We also injected mice with murine monoclonal IgG against native p210. Control groups were immunized with PADRE peptide alone or with control murine monoclonal IgG. Immunization with p210-PADRE induced an IgG1 antibody response against p210 that was associated with reduced atherosclerotic plaque formation in the aorta and reduced MDA-LDL content in the lesions. Treatment with monoclonal p210 IgG produced a similar reduction in atherosclerosis as immunization with p210-PADRE. Our findings support an atheroprotective role of antibodies against the apoB100 native p210 and suggest that vaccines that induce the expression of native p210 IgG represent a potential therapeutic strategy for lowering cardiovascular risk.

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