Helicobacter pylori and colorectal neoplasms: a concise review

Abstract

Helicobacter pylori is the main etiological agent of all malignant tumors caused by an infectious disease. It is a major, at times dominant, factor in the pathogenesis of a large spectrum of diseases such as acute and chronic gastritis, gastric and duodenal ulcers, gastric carcinoma, and lymphoma. Epidemiological and experimental studies suggest that H. pylori chronic infection may be related to different extragastric diseases, including colorectal neoplasms. This concise review aims to explore the association of H. pylori infection with colorectal cancer and adenoma, including the recent epidemiological findings, the diagnostic methods employed to detect H. pylori and virulent factors, and the potentially involved mechanisms. Furthermore, is attempted to establish the current data integration for causal inference using the Bradford-Hill causality criteria. The weak, although global, strength of the epidemiological positive association between H. pylori infection and colonic neoplasms associated to new mechanisms postulated to explain this interaction, including intestinal dysbiosis, should stimulate future studies. Prospective confirmatory studies to establish the role of H. pylori eradication in the process of carcinogenic transformation of the colonic epithelium may define its eventual role in the treatment and prevention of colonic neoplasms.

Exploring the Role of the Gut Microbiota in Colorectal Cancer Development

“…Besides its clear involvement in gastric carcinogenesis, recent studies have reported an association between Helicobacter pylori and CRC [42,43]. A study involving 812,736 individuals found that Helicobacter pylori infection is associated with an 18% higher risk of developing CRC and a 12% higher risk of death from CRC [44].…”

“…A study involving 812,736 individuals found that Helicobacter pylori infection is associated with an 18% higher risk of developing CRC and a 12% higher risk of death from CRC [44]. An explanation for this pathogenic relationship can be found in the disruption of cell proliferation caused by the vacA toxin, which is produced by Helicobacter pylori [43]. Ralser et al identified a specific immune pattern associated with Helicobacter pylori infection, characterized by a reduction in regulatory T cells and proinflammatory T cells [45].…”

Research Progress of Intestinal Microecology in the Pathogenesis of Colorectal Adenoma and Carcinogenesis

“… 98 Therefore, H pylori eradication might have an impact on the prevention of colorectal neoplasm formation. 99 , 100 …”

“…98 Therefore, H pylori eradication might have an impact on the prevention of colorectal neoplasm formation. 99,100 Based on our review, the diversity of the gut microbiota associated inflammatory responses, immune regulation, and metabolic changes have played an important role in the development and progression of colorectal adenomas (Figure 1).…”

Tumor Microenvironment Shapes Colorectal Cancer Progression, Metastasis, and Treatment Responses

“…In addition to gastric cancer, the association between H. pylori infection and CRC has also been reported ( 14 ), but the mechanism remains elusive. One possibility is that the vacA toxin produced by H. pylori results in cell proliferation dysregulation, and thus, induces CRC initiation and progression ( 15 ). Similarly, B. fragilis toxin (BFT) activates Wnt and NF-κB signaling, leading to DNA damage and the initiation and promotion of CRC ( 16 ).…”