Inflammatory Cytokines as Potential Inducements of Early Gastric Mucosal Lesions in Helicobacter pylori-Infected Patients.

BACKGROUND

Chronic inflammation due to Helicobacter pylori infection causes the development of many gastrointestinal diseases, such as gastric ulcer and atrophic gastritis. This study is aimed at investigating the relationship between inflammatory cytokines and pepsinogen levels in H. pylori-infected patients.

METHOD: A total of 165 H. pylori-infected subjects without atrophic gastritis were recruited, and their demographic, medical, and lifestyle information were collected. Inflammatory cytokines such as IL-8, IFN-γ, TNF-α, CRP, IL-17A, IL-1β, IL-18, and pepsinogen (PGs I and II) levels were measured. Multiple linear regression was used to analyze the relationship between cytokines and PG levels, whereas segmental regression explored threshold or saturation effects.

RESULT: IL-17A and IFN-γ were positively correlated with PG I and LNPG II, with each 1-pg/mL increase in IL-17A associated with a 2.595 (95% CI: 0.854, 4.335)-ng/mL increase in PG I and a 0.012 (95% CI: 0.002, 0.022)-ng/mL increase in LNPG II; each 1-pg/mL increase in IFN-γ was associated with a 1.746 (95% CI: 0.702, 2.791)-ng/mL increase in PG I and a 0.008 (95% CI: 0.002, 0.0191)-ng/mL increase in LNPG II. No significant correlation was found between inflammatory cytokines and the PG I/PG II ratio (PGR).

CONCLUSION

In H. pylori-infected patients without atrophic gastritis, IL-17A and IFN-γ levels showed a linear correlation with PG levels. These cytokines may be closely associated with early gastric mucosal lesions. However, further research is needed to elucidate their specific mechanisms in disease pathogenesis.