Association between Helicobacter pylori infection and carotid atherosclerosis in Chinese adults

Du, Liang; Liu, Jianghong; Jin, Cheng; Ma, Yuan; Yin, Linlin; Man, Sailimai; Li, Shijun; Li, Liming; Ning, Yi; Zhang, Xinghu

doi:10.1016/j.athplu.2021.08.004

Cited by 5 publications

(4 citation statements)

References 37 publications

(56 reference statements)

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“…MCs express a variety of TLRs that sense the presence of pathogens. MC expression of TLR, alteration in TLR expression, and possible endo-/exogenous agonists triggering MC activation are of the aspects of poorly illuminated participation of MCs in atherosclerosis [ 130 – 132 ] …”

Section: Unmet Questions In MC Involvement In Atherosclerosismentioning

confidence: 99%

Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization

Elieh-Ali-Komi,

Bot,

Rodríguez-González

et al. 2024

Clinic Rev Allerg Immunol

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Mast cells (MCs) are commonly recognized for their crucial involvement in the pathogenesis of allergic diseases, but over time, it has come to light that they also play a role in the pathophysiology of non-allergic disorders including atherosclerosis. The involvement of MCs in the pathology of atherosclerosis is supported by their accumulation in atherosclerotic plaques upon their progression and the association of intraplaque MC numbers with acute cardiovascular events. MCs that accumulate within the atherosclerotic plaque release a cocktail of mediators through which they contribute to neovascularization, plaque progression, instability, erosion, rupture, and thrombosis. At a molecular level, MC-released proteases, especially cathepsin G, degrade low-density lipoproteins (LDL) and mediate LDL fusion and binding of LDL to proteoglycans (PGs). Through a complicated network of chemokines including CXCL1, MCs promote the recruitment of among others CXCR2+ neutrophils, therefore, aggravating the inflammation of the plaque environment. Additionally, MCs produce extracellular traps which worsen inflammation and contribute to atherothrombosis. Altogether, evidence suggests that MCs actively, via several underlying mechanisms, contribute to atherosclerotic plaque destabilization and acute cardiovascular syndromes, thus, making the study of interventions to modulate MC activation an interesting target for cardiovascular medicine.

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Section: Unmet Questions In MC Involvement In Atherosclerosismentioning

confidence: 99%

Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization

Elieh-Ali-Komi,

Bot,

Rodríguez-González

et al. 2024

Clinic Rev Allerg Immunol

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“…pylori infection is linked to arterial stiffness, an early indicator of atherosclerosis associated with MetS-related AH and an independent predictor of CVD complications and all-cause fatality (21). Interestingly, the occurrence of H. pylori DNA in atherosclerotic plaques and the H. pylori infection-related carotid plaque onset in adults without previous CVD suggest that this bacterium could play a role in the pathogenesis of atherosclerosis and that its eradication may decrease the burden of MetS-related atherosclerosis (82)(83)(84). H. pylori infection has been associated with fatal MetS-related ischemic heart disease and stroke outcomes than with nonfatal events ascertained by general practitioners.…”

Section: H Pylori and Mets-related Cvdmentioning

confidence: 99%

Impact of Helicobacter pylori and metabolic syndrome-related mast cell activation on cardiovascular diseases

Doulberis,

Papaefthymiou,

Polyzos

et al. 2024

Front. Gastroenterol.

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Helicobacter pylori, a widely renowned bacterium, has recently gained attention owing to its potential impact on extragastric health. The emergence of research linking H. pylori infection with metabolic syndrome (MetS)-related cardiovascular diseases (CVDs) has raised intriguing questions about the pathogenic linkage and its translational implications for clinicians. MetS encompasses a collection of metabolic abnormalities that considerably elevate the risk of CVDs and cerebrovascular diseases. Emerging evidence supports a potential pathogenetic role of H. pylori for MetS-related disorders through mechanisms implicating chronic smoldering inflammation, insulin resistance (IR), and modulation of immune responses. One intriguing aspect of this possible connection is the role of mast cells (MCs), a subset of immune cells representing innate immune system effector cells. They play a fundamental role in innate immune responses and the modulation of adaptive immunity. Activated MCs are commonly found in patients with MetS-related CVD. Recent studies have also suggested that H. pylori infection may activate MCs, triggering the release of pro-inflammatory mediators that contribute to IR and atherosclerosis. Understanding these intricate interactions at the cellular level provides new insights into the development of therapeutic strategies targeting both H. pylori infection and MetS-related MCs activation. This review investigates the current state of research regarding the potential impact of H. pylori infection and MetS-related MCs activation on the pathophysiology of CVD, thereby opening up new avenues for related research and paving the way for innovative approaches to prevention and treatment in clinical practice

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“…Atherosclerosis originates from toxic damage to the vascular endothelium linked to the accumulation of lipids associated with a persistent inflammatory state that alters the production of nitric oxide [20][21][22][23][24][25] (Figure 1). Nitric oxide (NO) regulates the tone of smooth muscle cells and of the vascular wall in response to a stimulus that induces a vasodilatory action [25,26].…”

Section: Pathogenesis Of Atherosclerosis: the Centrality Of Endotheli...mentioning

confidence: 99%

“…HP is a Gram-negative bacterium, with a microaerophilic metabolism able to damage the mucosal barrier of the stomach, causing gastritis, peptic ulcer, and eventually gastric cancer [17]. Growing evidence has shown that HP infection is associated with extra gastric manifestations such as CVD, but other studies do not find this association significant [18][19][20]. Since there are conflicting opinions in the literature on the relationship between HP infection, chronic inflammatory state, and atherosclerosis, we believe that a more in-depth study of the evidence is needed.…”

Section: Introductionmentioning

confidence: 99%

Role of Helicobacter pylori Infection in Pathogenesis, Evolution, and Complication of Atherosclerotic Plaque

Ciarambino,

Crispino,

Minervini

et al. 2024

Biomedicines

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The therapeutic management of atherosclerosis focuses almost exclusively on the reduction of plasma cholesterol levels. An important role in the genesis and evolution of atherosclerosis is played by chronic inflammation in promoting thrombosis phenomena after atheroma rupture. This review aims to take stock of the knowledge so far accumulated on the role of endemic HP infection in atherosclerosis. The studies produced so far have demonstrated a causal relationship between Helicobacter pylori (HP) and CVD. In a previous study, we demonstrated in HP-positive patients that thrombin and plasma fragment 1 + 2 production was proportionally related to tumor necrosis factor-alpha levels and that eradication of the infection resulted in a reduction of inflammation. At the end of our review, we can state that HP slightly affects the risk of CVD, particularly if the infection is associated with cytotoxic damage, and HP screening could have a clinically significant role in patients with a high risk of CVD. Considering the high prevalence of HP infection, an infection screening could be of great clinical utility in patients at high risk of CVD.

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Association between Helicobacter pylori infection and carotid atherosclerosis in Chinese adults

Cited by 5 publications

References 37 publications

Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization

Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization

Impact of Helicobacter pylori and metabolic syndrome-related mast cell activation on cardiovascular diseases

Role of Helicobacter pylori Infection in Pathogenesis, Evolution, and Complication of Atherosclerotic Plaque

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