Virulence of Helicobacter pylori outer membrane proteins: an updated review

Abstract

Helicobacter pylori (H. pylori) infection is associated with some gastric diseases, such as gastritis, peptic ulcer, and gastric cancer. CagA and VacA are known virulence factors of H. pylori, which play a vital role in severe clinical outcomes. Additionally, the expression of outer membrane proteins (OMPs) helps H. pylori attach to gastric epithelial cells at the primary stage and increases the virulence of H. pylori. In this review, we have summarized the paralogs of H. pylori OMPs, their genomic loci, and the different receptors of OMPs identified so far. We focused on five OMPs, BabA (HopS), SabA (HopP), OipA (HopH), HopQ, and HopZ, and one family of OMPs: Hom. We highlight the coexpression of OMPs with other virulence factors and their relationship with clinical outcomes. In conclusion, OMPs are closely related to the pathogenic processes of adhesion, colonization, persistent infection, and severe clinical consequences. They are potential targets for the prevention and treatment of H. pylori-related diseases.

Nanomechanical Hallmarks of Helicobacter pylori Infection in Pediatric Patients

“…H. pylori infection usually occurs in childhood, and when untreated, remains present in the life of the host [ 3 , 6 , 11 ]. The infection is usually associated with asymptomatic gastritis, and in the long-term it may result in more severe clinical outcomes, such as gastric ulcer, duodenal ulcer, and gastric cancer [ 2 , 3 , 4 , 12 , 13 ]. This bacterium has various virulence factors, including a cytotoxin-associated gene A (CagA), a vacuolating cytotoxin A (VacA), and various outer membrane proteins that allow this microorganism to move around and survive in the unfavorable environment of the human stomach.…”

“…This bacterium has various virulence factors, including a cytotoxin-associated gene A (CagA), a vacuolating cytotoxin A (VacA), and various outer membrane proteins that allow this microorganism to move around and survive in the unfavorable environment of the human stomach. Moreover, CagA and VacA may deregulate the host’s intracellular signaling pathways, promoting neoplastic transformation [ 2 , 13 , 14 ]. CagA can interact with the host’s proteins to activate further signaling pathways, thereby activating the host’s inflammatory responses and cell proliferation.…”

Microbe-Driven Genotoxicity in Gastrointestinal Carcinogenesis

“…While a subpopulation of H. pylori is free-swimming in the mucus, some bacteria are able to attach to and colonize the intercellular junctions of epithelial cells. Several molecular adhesins, such as BabA, SabA and HopQ, have been described to be important for the attachment to epithelial cells [ 112 ]. Salama and colleagues found that the helical shape of H. pylori allows the bacterium not only to swim directedly in the mucus but also to interact with the host and induce inflammation [ 113 ].…”

Myricetin as an Antivirulence Compound Interfering with a Morphological Transformation into Coccoid Forms and Potentiating Activity of Antibiotics against Helicobacter pylori

“…Strains that produce multiple virulence factors are believed to have a greater potential to persistently infect the stomach [ 19 ]. The classically mentioned virulence determinants include urease [ 20 ], vacuolating toxin (VacA) [ 21 ], cytotoxic oncoprotein (CagA) [ 22 ], and numerous adhesins [ 23 ]. However, more and more often attention is paid to the morphological transformation of this bacterium as one of the key properties conditioning the survival of H. pylori [ 24 ].…”