Zhang HL, Niu XL, Wang N. Correlation of serum cytokine-induced neutrophil chemoattractant levels with Helicobacter pylori infection and disease severity in gastric cancer patients. World J Gastrointest Oncol 2025; 17(7): 105455 [DOI: 10.4251/wjgo.v17.i7.105455]
Corresponding Author of This Article
Ning Wang, Department of Gastroenterology, Shijiazhuang People's Hospital, No. 365 Jianhua South Street, Yuhua District, Shijiazhuang 050000, Hebei Province, China. zhangniuxh@163.com
Research Domain of This Article
Oncology
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Jul 15, 2025; 17(7): 105455 Published online Jul 15, 2025. doi: 10.4251/wjgo.v17.i7.105455
Correlation of serum cytokine-induced neutrophil chemoattractant levels with Helicobacter pylori infection and disease severity in gastric cancer patients
Hai-Ling Zhang, Xiao-Lei Niu, Ning Wang
Hai-Ling Zhang, Xiao-Lei Niu, Ning Wang, Department of Gastroenterology, Shijiazhuang People's Hospital, Shijiazhuang 050000, Hebei Province, China
Co-first authors: Hai-Ling Zhang and Xiao-Lei Niu.
Author contributions: Zhang HL, Niu XL and Wang N designed the experiments and conducted clinical data collection, performed postoperative follow-up and recorded the data; Wang N conducted the collation and statistical analysis, make critical revisions to important knowledge content; all authors read and approved the final manuscript. Zhang HL and Niu XL are co-first authors and contributed equally to this work, including design of the study, acquiring and analyzing data from experiments, and writing of the manuscript.
Supported by Hebei Province Medical Science Research Project Plan, No. 20210923.
Institutional review board statement: This study was approved by the Ethics Committee of Shijiazhuang People's Hospital.
Informed consent statement: The ethics committee of the institution exempted patients from informed consent.
Conflict-of-interest statement: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Data sharing statement: All data generated or analyzed during this study are included in this published article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ning Wang, Department of Gastroenterology, Shijiazhuang People's Hospital, No. 365 Jianhua South Street, Yuhua District, Shijiazhuang 050000, Hebei Province, China. zhangniuxh@163.com
Received: April 15, 2025 Revised: May 16, 2025 Accepted: June 18, 2025 Published online: July 15, 2025 Processing time: 89 Days and 17.4 Hours
Abstract
BACKGROUND
Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, with Helicobacter pylori (H. pylori) infection recognized as a major risk factor. Chronic H. pylori-induced inflammation drives carcinogenesis through neutrophil-mediated pathways, in which cytokine-induced neutrophil chemoattractant (CINC) plays a pivotal role. However, the interplay among H. pylori virulence factors, systemic CINC levels, and GC progression remains poorly defined.
AIM
To investigate the correlation among serum CINC levels, H. pylori infection, and disease severity in patients with GC.
METHODS
This retrospective cohort study included 258 patients with GC diagnosed between April 2020 and November 2023. H. pylori infection was confirmed via histology, rapid urease test, and serology. Serum CINC levels were quantified using ELISA. Statistical analyses were performed with SPSS 26.0.
RESULTS
The H. pylori-positive patients exhibited significantly higher serum CINC levels (312.5 ± 120.3 pg/mL) than the H. pylori-negative patients (150.2 ± 95.4 pg/mL; P < 0.05). CINC levels were correlated positively with TNM stage in the H. pylori-positive patients (P < 0.05), with the highest levels recorded in stage IV (415.7 ± 150.6 pg/mL). The patients infected with cytotoxin-associated gene A/vacuolating cytotoxin-positive H. pylori strains had elevated CINC levels (P < 0.05). High CINC levels and H. pylori infection independently predicted poor survival (HR of 2.41 and 1.89, respectively; P < 0.05).
CONCLUSION
Elevated serum CINC levels are strongly associated with H. pylori infection, advanced TNM staging, and poor prognosis in GC. CINC serves as a novel prognostic biomarker, underscoring the role of neutrophil-driven inflammation in H. pylori-associated carcinogenesis.
Core Tip: This study reveals that Helicobacter pylori (H. pylori) infection significantly elevates serum cytokine-induced neutrophil chemoattractant (CINC) levels in gastric cancer patients, particularly in those infected with cytotoxin-associated gene A/vacuolating cytotoxin-positive strains. CINC levels correlate with advanced TNM staging and independently predict poor survival, highlighting its role as a novel prognostic biomarker. Longitudinal monitoring demonstrates dynamic CINC changes aligned with disease progression, suggesting utility in treatment response assessment. These findings position CINC-driven neutrophilic inflammation as a therapeutic target and underscore the synergy between H. pylori virulence factors and systemic inflammation in accelerating gastric carcinogenesis.
