The quest for immunotherapy in atherosclerosis: CANTOS study, interleukin-1β and vascular inflammation

Bermúdez, Valmore; Rojas, Joselyn; Velasco, Manuel

doi:10.21037/jtd.2017.12.47

Cited by 7 publications

(4 citation statements)

References 22 publications

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“…The promising results of the CANTOS trial have rendered immunomodulation a new role for therapeutic approaches toward atherosclerosis. Immunomodulation in atherosclerosis can basically have three targets: anti-inflammation, cholesterol synthesis, and immunization against neoantigens [27]. Because multiple and various mediators have been involved in inflammation, one can assume that targeting only one specific mediator such as IL-1b might not inhibit all inflammatory pathways implicated in atherosclerotic development.…”

Section: Other Immunomodulatory Therapiesmentioning

confidence: 99%

Critical roles of inflammation in atherosclerosis

Moriya

2019

Journal of Cardiology

266

177

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There is accumulating evidence that vascular inflammation plays critical roles in pathophysiology of atherosclerosis. It is widely accepted that both innate and adaptive immune responses are important for initiation and progression of atherosclerosis, which mainly consist of monocytes, macrophages, neutrophils, T lymphocytes, and B lymphocytes. Moreover, inflammatory biomarkers such as high-sensitivity C-reactive protein and interleukin-6 are known to predict future cardiovascular events, as well as conventional low-density or high-density lipoprotein cholesterol. Thus, current understanding of the inflammatory mechanisms of atherosclerosis have led us to explore novel therapeutic approaches that reducing vascular inflammation itself could lower the rates of critical cardiovascular events. To address the inflammatory hypothesis of atherosclerosis, results of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) trial have been recently reported that anti-inflammatory therapy using canakinumab, a monoclonal antibody targeting interleukin-1β, significantly reduced recurrent cardiovascular events for secondary prevention of myocardial infarction at high inflammatory risk. In this review, we will first outline the mechanisms of atherosclerosis, especially focusing on their inflammatory aspects. Then we will introduce several critical inflammatory biomarkers that contribute to risk stratification of clinical cardiovascular events. Lastly, we will discuss potentiality and future perspectives of reducing inflammation as a novel therapeutic target for atherosclerotic cardiovascular diseases.

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Section: Other Immunomodulatory Therapiesmentioning

confidence: 99%

Critical roles of inflammation in atherosclerosis

Moriya

2019

Journal of Cardiology

266

177

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“…Interestingly, the susceptibility to ASCVD differs among these patients, even when LDL-C levels are similar [ 6 ], suggesting that a pathogenetic role for ASCVD may be played by other factors. Among them, chronic low-grade inflammation, via the activation of the nucleotide-binding domain; the leucine-rich containing family, pyrin domain-containing-3 (NLRP3) inflammasome/interleukin 1-β (IL1-β) pathway [ 7 , 8 ] is a very important player, as demonstrated by the CANTOS study [ 9 ]. Chronic inflammation is promoted by different conditions, including dysbiosis of the gut and oral microbiota [ 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Oral Porphyromonas gingivalis and Fusobacterium nucleatum Abundance in Subjects in Primary and Secondary Cardiovascular Prevention, with or without Heterozygous Familial Hypercholesterolemia

et al. 2022

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Background: Low-grade chronic inflammation, promoted by dysbiosis of the gut and oral microbiota, has been shown to contribute to individual susceptibility to atherosclerotic cardiovascular disease (ASCVD). High oral Porphyromonas gingivalis (Pg) and lower Fusobacterium nucleatum (Fn) concentrations have been associated with clinical and experimental atherosclerosis. We assessed oral Pg and Fn abundance in very high-risk patients with previously diagnosed ASCVD, with or without heterozygous familial hypercholesterolemia (HeFH), in subjects with HeFH in primary prevention and in healthy subjects. Methods: In this cross-sectional study, 40 patients with previously diagnosed ASCVD (10 with genetically proven HeFH, and 30 without FH), 26 subjects with HeFH in primary prevention, and 31 healthy subjects were selected to quantify oral Pg and Fn abundance by qPCR and assess oral health status. Results: Compared to healthy subjects, patients with previously diagnosed ASCVD showed greater Pg abundance (1101.3 vs. 192.4, p = 0.03), but similar Fn abundance. HeFH patients with ASCVD had an even greater Pg abundance than did non-HeFH patients and healthy subjects (1770.6 vs. 758.4 vs. 192.4, respectively; p = 0.048). No differences were found in the levels of Pg and Fn abundance in HeFH subjects in primary prevention, as compared to healthy subjects. Conclusions: Greater oral Pg abundance is present in very high-risk patients with previously diagnosed ASCVD, with or without FH, suggesting a potential relationship with CV events. Future studies will assess the predictive value of Pg abundance measurement in ASCVD risk stratification.

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“…IL-1β is an upstream factor in the inflammatory waterfall chain. This increases the expression of IL-1β canonical proinflammatory mediators like IL-6, IL-8, IL-1α, TNF-α, adhesion molecules, and MCP-1 ( Bermúdez et al, 2018 ). NLRP3 inflammasome plays an important role in foam cell death and chronic vascular inflammation.…”

Section: Anti-inflammatory Therapiesmentioning

confidence: 99%

Advances in immunotherapy modalities for atherosclerosis

Meng

Liu

et al. 2023

Front. Pharmacol.

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Cardiovascular disease (CVD) is one of the leading causes of death worldwide. Atherosclerosis is the pathological basis of atherosclerotic cardiovascular disease (ASCVD). Atherosclerosis is now understood to be a long-term immune-mediated inflammatory condition brought on by a complicated chain of factors, including endothelial dysfunction, lipid deposits in the artery wall, and monocyte-derived macrophage infiltration, in which both innate immunity and adaptive immunity play an indispensable role. Recent studies have shown that atherosclerosis can be alleviated by inducing a protective immune response through certain auto-antigens or exogenous antigens. Some clinical trials have also demonstrated that atherosclerotic is associated with the presence of immune cells and immune factors in the body. Therefore, immunotherapy is expected to be a new preventive and curative measure for atherosclerosis. In this review, we provide a summary overview of recent progress in the research of immune mechanisms of atherosclerosis and targeted therapeutic pathways.

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The quest for immunotherapy in atherosclerosis: CANTOS study, interleukin-1β and vascular inflammation

Cited by 7 publications

References 22 publications

Critical roles of inflammation in atherosclerosis

Critical roles of inflammation in atherosclerosis

Oral Porphyromonas gingivalis and Fusobacterium nucleatum Abundance in Subjects in Primary and Secondary Cardiovascular Prevention, with or without Heterozygous Familial Hypercholesterolemia

Advances in immunotherapy modalities for atherosclerosis

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