Abstract
BACKGROUND: Recently, the effects of Helicobacter pylori (H. pylori) infection on the prognosis of chronic atrophic gastritis (CAG) are still unclear. The aim of our study was to discuss the role of H. pylori infection on the prognosis of CAG by inducing the M1/M2 macrophage polarization. METHODS: A total of 180 subjects as control (group 1), CAG patients without H. pylori infection (group 2) and H. pylori-associated CAG patients (group 3) were respectively recruited for this cross-sectional investigation in Daqing Oilfield General Hospital from May 2019 to July 2020. Their serum samples were collected to determine the concentrations of pro-inflammatory and anti-inflammatory cytokines. Meanwhile, the gastric mucosa was excised to determine the related gene expressions on the M1/M2 macrophage polarization. Then the prognosis of CAG was evaluated according to the status of clinical manifestations and endoscopic examination after the follow-up. RESULTS: Notably, it was proved that compared with the control group, the expressions and concentrations of pro-inflammatory cytokines (M1 macrophage: inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin-6 (IL-6)) were significantly higher, while the anti-inflammatory cytokines (M2 macrophage: arginase-1 (Arg-1), IL-4 and IL-10) were apparently reduced in the group 2 and group 3 (P < 0.05). Moreover, more days were needed for the prognosis of CAG in group 3 than those in group 2, which was accompanied by higher expressions of pro-inflammatory and lower anti-inflammatory cytokines at the baseline (P < 0.05). Furthermore, negative correlations were shown between the concentrations of iNOS, TNF-α, IFN-γ and IL-6, and the prognosis of CAG (P < 0.05), while positive correlations were observed between the contents of IL-4 and IL-10, and prognosis of CAG (P < 0.05). CONCLUSION: These above results indicated that H. pylori infection-induced disorders of M1/M2 macrophage polarization could affect the prognosis of CAG.