An Overview of Helicobacter pylori Survival Tactics in the Hostile Human Stomach Environment

Abstract

Helicobacter pylori is well established as a causative agent for gastritis, peptic ulcer, and gastric cancer. Armed with various inimitable virulence factors, this Gram-negative bacterium is one of few microorganisms that is capable of circumventing the harsh environment of the stomach. The unique spiral structure, flagella, and outer membrane proteins accelerate H. pylori movement within the viscous gastric mucosal layers while facilitating its attachment to the epithelial cells. Furthermore, secretion of urease from H. pylori eases the acidic pH within the stomach, thus creating a niche for bacteria survival and replication. Upon gaining a foothold in the gastric epithelial lining, bacterial protein CagA is injected into host cells through a type IV secretion system (T4SS), which together with VacA, damage the gastric epithelial cells. H. pylori does not only establishes colonization in the stomach, but also manipulates the host immune system to permit long-term persistence. Prolonged H. pylori infection causes chronic inflammation that precedes gastric cancer. The current review provides a brief outlook on H. pylori survival tactics, bacterial-host interaction and their importance in therapeutic intervention as well as vaccine development.

Innate Immunity Crosstalk with Helicobacter pylori: Pattern Recognition Receptors and Cellular Responses

“…The immune response against H. pylori is initiated across gastric epithelial cells (GECs), either through the signaling or recruitment by activated GEC or through the direct recognition of various bacterial components or virulence factors [ 45 ]. This causes a cascade of innate immune cell activation by neutrophils, macrophages, and dendritic cells.…”

Relationship between Helicobacter pylori infection and gastrointestinal microecology

“…This phenomenon further shows that H. pylori has advantages over other flora. It is not clear why H. pylori infection changes the gastric microecology, although possible reasons have been postulated ( Cheok et al., 2021 ): H. pylori changes the gastric microenvironment, and the ammonia and bicarbonate produced by decomposing urea can also serve as substrates for other microbial communities; H. pylori infection induces the regulation of the H+/K+-ATPase D subunit promoter by the Nuclear Factor- Kappa B (NF-kB) P50 homologous dimer, which downregulates the expression of H+/K+-ATPase mRNA, and inhibits gastric acid secretion, thereby increasing gastric pH and creating favorable conditions for the colonization of other microorganisms; H. pylori can induce the production of cytokines and antimicrobial peptides, thereby leading to chronic gastritis and inhibiting other local microorganisms; H. pylori may directly alter the mucosal barrier by changing the expression of gastric mucin; H. pylori can alter the lifestyle and dietary patterns of its subjects; H. pylori can develop T regulatory-mediated tolerance to other bacterium, and suppress the effector T-cell responses ( Sung et al., 2020 ; Marginean et al., 2021 ).…”

Comparison of Different Histological Staining Methods for Detection of Helicobacter pylori Infection in Gastric Biopsy

“…It is responsible for the onset of several gastric pathologies ranging from gastritis to gastric carcinoma [ 2 ]. It is a well-defined spiral-shaped, gram-negative bacteria [ 3 ]. This microorganism was first discovered by Marshall et al [ 4 ].…”