Neutrophil‐Mediated Mechanisms and Therapeutic Reversibility of Gastric Intestinal Metaplasia

Gastric intestinal metaplasia (GIM), a precancerous gastric lesion, represents a critical transitional stage in the Correa cascade that progresses from chronic inflammation to gastric adenocarcinoma (GAC). Emerging evidence implicates neutrophils as key orchestrators of GIM pathogenesis through multifaceted interactions within the tumor microenvironment. Therapeutic strategies targeting neutrophil activation, migration, and effector functions, including autophagy modulation and phenotypic reprogramming to an anti-inflammatory N2 state, hold promise in reversing GIM progression. This review synthesizes the current knowledge on neutrophil-mediated mechanisms and explores clinically actionable pathways for GIM reversibility.