**Abstract**

The etiologic link between *H. pylori* infection and gastric chronic inflammation and related complications has been well established, but pathogenic pathways are still widely discussed and not sufficiently clear. The introduction of cultureindependent molecular techniques has allowed better understanding of the gastric microbiota and has revealed that, when present, *H. pylori* represents the main colonizer but is part of a far more complex and dynamic microbiota than previously thought. This conceptual shift has made way for new pathogenic theories, focused on the interrelations between *H. pylori* and other gastric microbiota. Main factors that affect the gastric microbiota are gastric acidity, inflammation, and environmental factors, such as diet and drugs. Previous studies have made progress in explaining the complex interactions between gastric microorganisms in healthy individuals and their role in the development of related gastroduodenal (peptic ulcers and gastric cancer (GC)) and extraintestinal diseases, but more scientific proof is needed. This review presents current knowledge on gastric microbiota and its role in health and in the development of gastroduodenal diseases.

**Keywords:** gastric microbiota, *H. pylori*, pathogenesis, chronic inflammation, peptic ulcers, gastric cancer

### **1. Introduction**

The first isolation of *Helicobacter pylori* (*H. pylori*) in 1982 [1] changed the traditional misconception that the stomach, with its naturally hostile environment, cannot be a reservoir for microbial species. Since then *H. pylori* has been well established as a key factor in gastric pathology, being the main cause of chronic active gastritis. This inflammation can progress to often interlinked severe complications such as atrophic gastritis, peptic ulcer disease, and gastric malignancies [2]. The assumption of the uniqueness of *H. pylori* as the only bacteria able to survive in the gastric hostile environment has also fast been shattered with the advances in culture-dependent and culture-independent techniques that revealed that *H. pylori* is part of a complex gastric microbiota. The gastric microbial density is now estimated at around 102 to 104 colony-forming units (CFU)/mL [3], with variations related to local pH, site of isolation, and environmental factors, such as food ingestion and medication intake. Furthermore, the pool of species and subspecies varies related to *H. pylori* status and related pathologic complications. Due to this multitude of factors, the differentiation between resident and transient microbiota and its role in health and disease remains controversial. Nevertheless, the potential of understanding the structure and dynamics of the gastric microbiota for the pathogenesis, diagnosis, and treatment of gastroduodenal diseases remains. Hence, this review aims to underline current knowledge on gastric microbiota and its relation to gastroduodenal pathology.
