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. 2023 Sep 9;9(9):e20037.
doi: 10.1016/j.heliyon.2023.e20037. eCollection 2023 Sep.

Helicobacter pylori infection increases the risk of carotid plaque formation: Clinical samples combined with bioinformatics analysis

Yi Chen  1 , Ningning You  1 , Chaoyu Yang  1 , Jinshun Zhang  2
Affiliations

Helicobacter pylori infection increases the risk of carotid plaque formation: Clinical samples combined with bioinformatics analysis

Yi Chen et al. Heliyon. .

Abstract

Objective: Infection 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.

Methods: A 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.

Results: H. 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.

Keywords: Bioinformatics analysis; Carotid plaque; Gene expression; Helicobacter pylori; Immune microenvironment.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Construction of coexpression network of H. pylori infection and arterial plaque progression. (A, B) Selection of the optimal soft threshold in GSE27411 and GSE28829 datasets. (C, D) Division of different modules in GSE27411 and GSE28829 datasets. (E, F) Correlation between modules and diseases in GSE27411 and GSE28829 datasets.
Fig. 2
Fig. 2
Enrichment analysis of genes related to H. pylori infection and plaque progression. (A) Intersection gene of black module and turquoise module. (B) Go enrichment analysis of intersection genes. (C) KEGG enrichment analysis of intersection genes.
Fig. 3
Fig. 3
Identification of differential genes and hub genes. (A) Differential genes in GSE27411 dataset. (B) Differential genes in GSE28829 dataset. (C) Overlapping genes of modular genes and differential genes.
Fig. 4
Fig. 4
Expression of hub gene in H. pylori infected patients and patients with advanced plaque formation. (A) Expression of hub gene in GSE27411 dataset. (B) Expression of hub gene in GSE28829 dataset.
Fig. 5
Fig. 5
Immune cell infiltration among different samples. (A) Heatmap of distribution of different immune cells in GSE27411 dataset. (B) Difference of immune cells between H. pylori infected patients and normal people. (C) Heatmap of distribution of different immune cells in GSE28829 dataset. (D) Difference of immune cells between EA patients and AA patients.
Fig. 6
Fig. 6
Relationship between hub gene and immune cells. (A) Relationship between hub gene and immune cells in GSE27411 dataset. (B) Relationship between hub gene and immune cells in GSE28829 dataset.
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