Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms

Abstract

Helicobacter pylori is an organism associated with ulcer disease and gastric cancer. The latter is one of the most prevalent malignancies and currently the fourth major cause of cancer-related deaths globally. The pathogen infects about 50% of the world population, and currently, no treatment ensures its total elimination. There has been an increase in our understanding of the pathophysiology and pathogenesis mechanisms of H. pylori over the years. H. pylori can induce several genetic alterations, express numerous virulence factors, and trigger diverse adaptive mechanisms during its adherence and colonization. For successful colonization and infection establishment, several effector proteins/toxins are released by the organism. Evidence is also available reporting spiral to coccoid transition as a unique tactic H. pylori uses to survive in the host’s gastrointestinal tract (GIT). Thus, the virulence and pathogenicity of H. pylori are under the control of complex interplay between the virulence factors, host, and environmental factors. Expounding the role of the various virulence factors in H. pylori pathogenesis and clinical outcomes is crucial for vaccine development and in providing and developing a more effective therapeutic intervention. Here we critically reflect on H. pylori infection and delineate what is currently known about the virulence and pathogenesis mechanisms of H. pylori .

The Effects of Helicobacter pylori Infection on Gastric Microbiota in Children With Duodenal Ulcer

“…The close relationship between H. pylori infection and peptic ulcers has long been known. For example, 94% of patients with gastric ulcer and 98% of patients with duodenal ulcer have an associated H. pylori infection ( Chen et al, 2018 ), and ulcer recurrence was reduced after H. pylori eradication therapy ( Sharndama and Mba, 2022 ). Both innate and adaptive immune responses play a key role in the host’s response to H. pylori infection, but the crosstalk between H. pylori and the immune system in pediatric patients is far to be fully understood ( Mărginean et al, 2021 ).…”

Seroprevalence of Helicobacter Pylori in Plaque Psoriasis at Tertiary Care Hospital

“…Once H. pylori colonizes the gastric mucosa it initiates a strong inflammatory reaction, leading to alteration and uncontrolled release of systemic inflammatory mediators like interleukins; hence producing widespread systemic effects. These altered immunological mechanisms involve cellmediated and humoral immune reactions 12,13 . Staphlococcocal infection has since long been implicated as a triggering factor for the development of psoriasis through the role of superantigens.…”

Flagella at the Host-Microbe Interface: Key Functions Intersect With Redundant Responses

“…Although many different pathogens utilize flagellar motility within the host, it often provides varying degrees of fitness advantage and is not always necessary for host colonization. For example, the use of flagellar motility is integral to the pathogenesis strategy of Helicobacter pylori and Campylobacter jejuni , as evidenced by its absence hindering their ability to effectively colonize the host ( 1 , 27 , 32 – 35 ). By comparison, Salmonella enterica serovar Typhimurium (STM), Escherichia coli , and Pseudomonas aeruginosa selectively express their flagella at specific times and sites within the host to gain advantage over other members of the microbiota; however, these bacteria ultimately do not require flagellar motility for pathogenesis, and when expressed at the “wrong” time can actually impair colonization of the host ( 1 , 27 , 36 – 42 ).…”