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Helicobacter pylori infection selectively increases the risk for carotid atherosclerosis in young males.

ABSTRACT: BACKGROUND AND AIMS:Atherosclerosis is an important contributing factor to cardiovascular mortality. The role of Helicobacter pylori (H. pylori) infection in atherosclerosis is inconsistent and sometimes controversial. The present study aimed to determine if H. pylori infection is associated with carotid atherosclerosis. METHODS:17,613 males and females with both carotid ultrasonic examination and 13C-urea breath test for H. pylori infection were screened by a major Chinese university hospital from March 2012 to March 2017 for the study. Baseline demographics, cardiac risk factors, and laboratory studies were obtained. After exclusion for pre-specified conditions, 12,836 individuals were included in the analysis, including 8157 men (63.5%) and 4679 women (36.5%). Analysis was also made for 5-year follow-up data of 1216 subjects (869 males and 347 females) with and without H. pylori infection for development and progression of carotid atherosclerosis. RESULTS:After adjusting for age, sex, body mass index, lipid profile, hypertension, renal function, diabetes mellitus, and smoking, H. pylori infection was found as an independent risk factor for carotid atherosclerosis in males under 50 years, but not in older males or females (odds ratio 1.229, 95% CI 1.054-1.434, p?=?0.009). Follow-up data analysis showed that the incidence of carotid atherosclerosis from no atherosclerosis to detectable lesions was significantly higher in young males with persistent H. pylori infection than those without H. pylori infection (p?=?0.028) after 3 years. CONCLUSIONS:These data suggest that H. pylori infection might be an important risk factor for carotid atherosclerosis in young Chinese males under 50.

SUBMITTER: Zhang L

PROVIDER: S-EPMC7349937 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Helicobacter pylori infection selectively increases the risk for carotid atherosclerosis in young males.

Zhang Linfang L Chen Zhiheng Z Xia Xiujuan X Chi Jingshu J Li Huan H Liu Xiaoming X Li Rong R Li Yixi Y Liu Da D Tian Delin D Wang Hui H Petroski Greg F GF Flaker Greg C GC Hao Hong H Liu Zhenguo Z Xu Canxia C

Atherosclerosis 20191011

<h4>Background and aims</h4>Atherosclerosis is an important contributing factor to cardiovascular mortality. The role of Helicobacter pylori (H. pylori) infection in atherosclerosis is inconsistent and sometimes controversial. The present study aimed to determine if H. pylori infection is associated with carotid atherosclerosis.<h4>Methods</h4>17,613 males and females with both carotid ultrasonic examination and <sup>13</sup>C-urea breath test for H. pylori infection were screened by a major Chi ...[more]

PMID: 31704553

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Project description:ObjectiveInfection with Helicobacter pylori (H. pylori) may increase atherosclerosis, which can lead to carotid plaque formation. Our study examined the relationship between H. pylori infection and carotid plaque formation, and its underlying mechanisms.MethodsA total of 36,470 people who underwent physical examination in Taizhou Hospital Health Examination Center from June 2017 to June 2022 were included in this study. All people participated in the urease test, neck ultrasound, blood pressure detection, anthropometric measurement and biochemical laboratory examination. In addition, the GSE27411 and GSE28829 datasets in the Gene Expression Omnibus (GEO) database were used to analyze the mechanism of H. pylori infection and atherosclerosis progression.ResultsH. pylori infection, sex, age, blood lipids, blood pressure, fasting blood glucose, glycated hemoglobin and body mass index were risk factors for carotid plaque formation. An independent risk factor was still evident in the multivariate logistic regression analysis, indicating H. pylori infection. Furthermore, after weighted gene coexpression network analysis (WGCNA), we discovered 555 genes linked to both H. pylori infection and the advancement of atherosclerosis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed a strong correlation between these genes and immunity, infection, and immune disorders. SsGSEA analysis showed that H. pylori infection and atherosclerosis included changes in the immune microenvironment. Finally, three genes MS4A6A, ADAMDEC1 and AQP9 were identified to be involved in the formation of atherosclerosis after H. pylori infection. Conclusion: Our research affirms that H. pylori is a unique contributor to the formation of carotid plaque, examines the immune microenvironment associated with H. pylori infection and advanced carotid atherosclerosis, and offers fresh perspectives on how H. pylori infection leads to atherosclerosis.

Project description:A number of viruses and bacterial species have been implicated as contributors to atherosclerosis, potentially providing novel pathways for prevention. Epidemiological studies examining the association between Helicobacter pylori and cardiovascular disease have yielded variable results and no studies have been conducted in nonhuman primates. In this investigation, we examined the relationship between H. pylori infection and atherosclerosis development in socially housed, pre- and postmenopausal cynomolgus macaques consuming human-like diets. Ninety-four premenopausal cynomolgus monkeys (Macaca fascicularis) were fed for 36 months an atherogenic diet deriving its protein from either casein lactalbumin(CL) or high isoflavone soy (SOY). Animals were then ovariectomized and fed either the same or the alternate diet for an additional 36 months. Iliac artery biopsies were obtained at the time of ovariectomy and iliac and coronary artery sections were examined at the end of the study. Evidence of H. pylori infection was found in 64% of the monkeys and 46% of animals had live H. pylori within coronary atheromas as determined by mRNA-specific in situ hybridization. There was a significant linear relationship between the densities of gastric and atheroma organisms. Helicobactor pylori infection correlated with increased intimal plaque area and thickness at both the premenopausal and postmenopausal time points and regardless of diet (p< 0.01), although animals consuming the SOY diet throughout had the least amount of atherosclerosis. Additionally, plasma lipid profiles, intimal collagen accumulation, ICAM-1, and plaque macrophage densities were adversely affected by H. pylori infection among animals consuming the CL diet, while the SOY diet had the opposite effect. Plaque measurements were more highly associated with the densities of cagA-positive H. pylori within coronary atheromas than with the densities of gastric organisms, whereas plasma lipid changes were associated with H. pylori infection, but not cagA status. This study provides strong evidence that live H. pylori infects atheromas, exacerbates atherosclerotic plaque development, and alters plasma lipid profiles independently of diet or hormonal status. Finally, socially subordinate animals relative to their dominant counterparts had a greater prevalence of H. pylori, suggesting a stress effect. The results indicate that early H. pylori eradication could prevent or delay development of cardiovascular disease.

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Helicobacter pylori infection selectively increases the risk for carotid atherosclerosis in young males.

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Helicobacter pylori infection selectively increases the risk for carotid atherosclerosis in young males.

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