Published online Jul 15, 2025. doi: 10.4251/wjgo.v17.i7.105455
Revised: May 16, 2025
Accepted: June 18, 2025
Published online: July 15, 2025
Processing time: 90 Days and 3.9 Hours
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.
To investigate the correlation among serum CINC levels, H. pylori infection, and disease severity in patients with GC.
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.
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/vacuo
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.
