Helicobacter pylori and colorectal neoplasia with emphasis on microbial mechanisms and causal evidence
- 1epartment of Gastroenterology, The People’s Hospital of Danyang, Affiliated Danyang Hospital of Nantong University, Zhenjiang, Jiangsu, China
Abstract
Helicobacter pylori (H. pylori) infection is associated with colorectal neoplasia in many observational studies, but a causal relationship and a preventive effect of eradication remain unestablished. This narrative review integrates clinical, microbial, experimental, and treatment evidence using four questions: which infection phenotype was measured, whether exposure preceded the colorectal outcome, whether a proposed intermediate was experimentally perturbed, and whether a defined intervention changed that outcome. Positive observational syntheses contrast with weaker or inconsistent prospective serological and genetic findings. Residual confounding, including socioeconomic and lifestyle differences, and non-equivalent exposure measurements limit causal interpretation. Gastric atrophy, endocrine changes, microbial remodeling, metabolites, and immune responses provide candidate links, but no complete infection-to-neoplasia sequence has been demonstrated in humans. Microbiota-dependent tumor promotion in genetically susceptible mice provides experimental support within that setting, whereas reduced tumor formation in an inflammation-driven model limits generalization. Neither model reproduces the duration and heterogeneity of human infection. Eradication findings depend on comparator selection, sufficient latency, and separation of randomized treatment assignment from successful clearance. A comparative appraisal links each proposed mechanism to its strongest available evidence, unresolved human causal link, and required validation. Infection status alone is not established as a basis for changing colorectal screening or claiming colorectal cancer prevention through eradication. Longitudinal human sampling, targeted tests of candidate intermediates, and long-term intervention analyses with explicit treatment comparisons are needed to establish clinical relevance.
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BibTeX
@article{xu2026helicobacter,
title = {{Helicobacter pylori and colorectal neoplasia with emphasis on microbial mechanisms and causal evidence}},
author = {Jian Xu},
journal = {Frontiers in Cellular and Infection Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fcimb.2026.1996461},
url = {https://doi.org/10.3389/fcimb.2026.1996461},
note = {CC BY},
}
RIS
TY - JOUR
TI - Helicobacter pylori and colorectal neoplasia with emphasis on microbial mechanisms and causal evidence
AU - Jian Xu
PY - 2026
DA - 2026/10/23
JO - Frontiers in Cellular and Infection Microbiology
DO - 10.3389/fcimb.2026.1996461
UR - https://doi.org/10.3389/fcimb.2026.1996461
AB - Helicobacter pylori (H. pylori) infection is associated with colorectal neoplasia in many observational studies, but a causal relationship and a preventive effect of eradication remain unestablished. This narrative review integrates clinical, microbial, experimental, and treatment evidence using four questions: which infection phenotype was measured, whether exposure preceded the colorectal outcome, whether a proposed intermediate was experimentally perturbed, and whether a defined intervention changed that outcome. Positive observational syntheses contrast with weaker or inconsistent prospective serological and genetic findings. Residual confounding, including socioeconomic and lifestyle differences, and non-equivalent exposure measurements limit causal interpretation. Gastric atrophy, endocrine changes, microbial remodeling, metabolites, and immune responses provide candidate links, but no complete infection-to-neoplasia sequence has been demonstrated in humans. Microbiota-dependent tumor promotion in genetically susceptible mice provides experimental support within that setting, whereas reduced tumor formation in an inflammation-driven model limits generalization. Neither model reproduces the duration and heterogeneity of human infection. Eradication findings depend on comparator selection, sufficient latency, and separation of randomized treatment assignment from successful clearance. A comparative appraisal links each proposed mechanism to its strongest available evidence, unresolved human causal link, and required validation. Infection status alone is not established as a basis for changing colorectal screening or claiming colorectal cancer prevention through eradication. Longitudinal human sampling, targeted tests of candidate intermediates, and long-term intervention analyses with explicit treatment comparisons are needed to establish clinical relevance.
SN - 2235-2988
ER -