Excerpt
The gastric mucosa is constantly exposed to a harsh environment due to numerous factors, including abrasion from consumed food, damage from orally administered drugs, digestive factors produced by mucosal epithelial cells including gastric acid and pepsinogen, ischemia and other stressors, and infection with
Helicobacter pylori. To meet these daunting challenges, the stomach has numerous mucosal defense mechanisms that prevent mucosal damage and maintain mucosal integrity [
1]. Mucosal injury occurs when damaging factors overwhelm defensive factors or when mucosal defense mechanisms, per se, are impaired [
1]. Gastric acid hypersecretion, the repeated ingestion of high salt-containing foods or nonsteroidal anti-inflammatory drugs (NSAIDs), and/or
H. pylori infection can result in superficial injury or deep ulceration of the mucosa manifest as erosions or peptic ulcers that usually heal after the insult is removed. Despite the decreasing incidence of peptic ulcers in the past 20 years, largely attributed to the use of proton pump inhibitors to inhibit acid secretion and the eradication of
H. pylori, peptic ulcers are still diagnosed in 5–10% of the general population [
2,
3]. Furthermore, even after treatment for
H. pylori infection, there is a cumulative 20% probability of ulcer recurrence within 6 months [
4] with the 5-year cumulative probability of ulcer recurrence in the absence of
H. pylori infection > 35% [
5]. Despite active work to understand factors that facilitate the initiation of or protection against ulceration, mechanisms that regulate the recurrence (relapse) of previously healed ulcers are largely unknown. …
