IL1B and chronic atrophic gastritis: Contributing to this effect is the IL-1β-dependent expression of IL-8, which, through a positive feedback loop and drives enhanced gastric IL-1β expression, culminating in enhanced mucosal inflammation [54] and low gastric acid output, which are necessary precursor steps for gastric atrophy [55], hyperplasia and GC [20], even in the absence of an adaptive immune system [56].