<scp><i>VacA</i></scp> genotypes and <scp>cagA‐EPIYA‐C</scp> motifs of <i>Helicobacter pylori</i> and gastric histopathological lesions

Khadir, Mounia El; Alaoui, Samia; Benajah, Dafr-Allah; Ibrahimi, Sidi Adil; Chbani, Laïla; Abkari, M. El; Bennani, Bahia

doi:10.1002/ijc.33158

Cited by 15 publications

(9 citation statements)

References 48 publications

(98 reference statements)

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“…The vacA subtypes: s1as1bm2, s2 m2 and m2, s1bm2 were significantly correlated to gastritis, whereas, subtypes s1am1 , s1am2 , m1 were significantly associated with gastric and duodenal ulcers ( 12 ). A present study reveals a significant association between the strains carrying the vacA m1 alleles and intestinal metaplasia in addition to gastric cancer ( 61 ). In this study, the vacA genotypes of the 85 H. pylori strains were diverse, but s1c/m1b (30.6%) and s1c/m2 (41.2%) were the dominant genotypes and the most frequent combination in chronic non-atrophic gastritis.…”

Section: Discussionmentioning

confidence: 53%

Correlation analysis of gastric mucosal lesions with Helicobacter pylori infection and its virulence genotype in Guiyang, Guizhou province, China

Hu¹,

Wang²,

Mi³

et al. 2022

Ann Transl Med

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Background: Helicobacter Pylori (H. pylori) infection is the most important factor affecting clinical outcome in patients with gastric mucosal lesions. This study aimed to investigate H. pylori infection in patients with gastric mucosal lesions and their virulence genotype in Guiyang, China.Methods: Pathological examinations of 1,364 biopsies from patients with upper gastrointestinal symptoms and H. pylori infection were analyzed according to different pathological types. The bacterial genome DNA was extracted from H. pylori strains isolated from gastric biopsies, and the cagA, vacA, and iceA virulence genes were detected and typed to analyze the correlation of their genotypes between different pathological lesions. Results:The positive rate of H. pylori infection was approximately 19.9% (272/1,364), as determined by histopathological examination (HPE). It was more frequently detected in men than in women. A total of 85 H. pylori isolates were obtained from 280 clinical samples (positive rate 30.4%, 85/280). Of these 85 strains, cagA, vacA, and iceA genes were identified in 85.9%, 100%, and 83.5% of samples, respectively. Approximately 74.1% of strains were cagA East Asian type (cagA-ABD), and 11.8% of were cagA Western strains (cagA-AB, cagA-ABC), only present in patients with chronic non-atrophic gastritis. Gastric intraepithelial neoplasia and gastric cancer harbored both Asian strains. A total of 7 combinations of vacA genotypes were noted, among which s1c/m1b (30.6%) and s1c/m2 (41.2%) were the dominant genotypes. The predominant iceA genotype was iceA1 (64.7%). Conclusions:We observed that the positive rate of H. pylori infection was related to the pathological type of patients' gastric mucosal lesions. Isolated H. pylori strains showed a unique genotype, mainly East Asian type cagA (ABD), vacA s1c/m2 genotype, and iceA1. These results provide an important reference for further studies of H. pylori in Guizhou province, China.

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Section: Discussionmentioning

confidence: 53%

Correlation analysis of gastric mucosal lesions with Helicobacter pylori infection and its virulence genotype in Guiyang, Guizhou province, China

Hu¹,

Wang²,

Mi³

et al. 2022

Ann Transl Med

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“…H. pylori is a major risk factor for gastric cancer [ 98 ]. Studies have shown that approximately 2% ~ 3% of people infected with H. pylori eventually develop gastric cancer [ 99 ]. Studies have also shown that autophagy can be induced by the concerted action of H. pylori and virulence factors in tumor cells [ 100 ].…”

Section: Crosstalk Between Microbiota and Autophagy In Cancer Developmentmentioning

confidence: 99%

Crosstalk between autophagy and microbiota in cancer progression

Wang

et al. 2021

Mol Cancer

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Autophagy is a highly conserved catabolic process seen in eukaryotes and is essentially a lysosome-dependent protein degradation pathway. The dysregulation of autophagy is often associated with the pathogenesis of numerous types of cancers, and can not only promote the survival of cancer but also trigger the tumor cell death. During cancer development, the microbial community might predispose cells to tumorigenesis by promoting mucosal inflammation, causing systemic disorders, and may also regulate the immune response to cancer. The complex relationship between autophagy and microorganisms can protect the body by activating the immune system. In addition, autophagy and microorganisms can crosstalk with each other in multifaceted ways to influence various physiological and pathological responses involved in cancer progression. Various molecular mechanisms, correlating the microbiota disorders and autophagy activation, control the outcomes of protumor or antitumor responses, which depend on the cancer type, tumor microenvironment and disease stage. In this review, we mainly emphasize the leading role of autophagy during the interaction between pathogenic microorganisms and human cancers and investigate the various molecular mechanisms by which autophagy modulates such complicated biological processes. Moreover, we also highlight the possibility of curing cancers with multiple molecular agents targeting the microbiota/autophagy axis. Finally, we summarize the emerging clinical trials investigating the therapeutic potential of targeting either autophagy or microbiota as anticancer strategies, although the crosstalk between them has not been explored thoroughly.

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“…6 Chronic infection with H. pylori exposes the gastric mucosa to various bacterial components such as lipopolysaccharide (LPS), outer membrane vesicles (OMVs), and toxic proteins. [7][8][9][10][11] The LPS from H. pylori can impair the expression of EGF and trigger the phosphorylation of STAT3, leading to gastric mucosal damage and chronic inflammation. 9 The OMVs produced by H. pylori can stimulate the mTOR signaling pathway to promote cell proliferation and carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

The role of toll‐like receptors in immune tolerance induced by Helicobacter pylori infection

Zhang,

Yan

et al. 2023

Helicobacter

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Helicobacter pylori (H. pylori) is a gram‐negative, microaerobic bacterium that colonizes the gastric mucosa in about half of the world's population. H. pylori infection can lead to various diseases. Chronic infection by H. pylori exposes the gastric mucosa to bacterial components such as lipopolysaccharide (LPS), outer membrane vesicles (OMVs), and several toxic proteins. Infected with H. pylori activates the release of pro‐inflammatory factors and triggers inflammatory responses that damage the gastric mucosa. As the only microorganism that permanently colonizes the human stomach, H. pylori can suppress host immunity to achieve long‐term colonization. Toll‐like receptors (TLRs) play a crucial role in T‐cell activation, promoting innate immune responses and immune tolerance during H. pylori infection. Among the 10 TLRs found in humans, TLR2, TLR4, TLR5, and TLR9 have been thoroughly investigated in relation to H. pylori‐linked immune regulation. In the present review, we provide a comprehensive analysis of the various mechanisms employed by different TLRs in the induction of immune tolerance upon H. pylori infection, which will contribute to the research of pathogenic mechanism of H. pylori.

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VacA genotypes and cagA‐EPIYA‐C motifs of Helicobacter pylori and gastric histopathological lesions

Cited by 15 publications

References 48 publications

Correlation analysis of gastric mucosal lesions with Helicobacter pylori infection and its virulence genotype in Guiyang, Guizhou province, China

Correlation analysis of gastric mucosal lesions with Helicobacter pylori infection and its virulence genotype in Guiyang, Guizhou province, China

Crosstalk between autophagy and microbiota in cancer progression

The role of toll‐like receptors in immune tolerance induced by Helicobacter pylori infection

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