Emerging Novel Virulence Factors of Helicobacter pylori

Weßler, Silja

doi:10.1007/978-4-431-55936-8_7

Cited by 2 publications

(3 citation statements)

References 118 publications

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“…The apoptotic effect on the host cells has been recognised for H. pylori and H. suis GGT (167). However, it seems that GGT is not the main factor in the induction of H. pylori -mediated apoptosis in T cells because a GGT-negative mutant still induces T-cell apoptosis (168). H. pylori GGT induces cell cycle arrest at the G1/S phase transition in T cells and gastric epithelial cells, and subsequently inhibits their proliferation (169, 170).…”

Section: The Genome and Virulence Factors Of H Pylorimentioning

confidence: 99%

“…H. pylori GGT induces cell cycle arrest at the G1/S phase transition in T cells and gastric epithelial cells, and subsequently inhibits their proliferation (169, 170). It was demonstrated that GGT and VacA could inhibit T cells which emphasises the role of secreted virulence factors in the H. pylori pathogenesis (168). GGT and VacA promote immune tolerance and gastric persistence that facilitate the prevention of asthma in vivo (165, 171).…”

Section: The Genome and Virulence Factors Of H Pylorimentioning

confidence: 99%

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Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

Mohammadzadeh,

Menbari,

Pishdadian

et al. 2023

Expert Rev. Mol. Med.

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Helicobacter pylori (H. pylori) is a worldwide spread bacterium, co-evolving with humans for at least 100 000 years. Despite the uncertainty about the mode of H. pylori transmission, the development of intra-gastric and extra-gastric diseases is attributed to this bacterium. The morphological transformation and production of heterogenic virulence factors enable H. pylori to overcome the harsh stomach environment. Using numerous potent disease-associated virulence factors makes H. pylori a prominent pathogenic bacterium. These bacterial determinants are adhesins (e.g., blood group antigen-binding adhesin (BabA)/sialic acid-binding adhesin (SabA)), enzymes (e.g., urease), toxins (e.g., vacuolating cytotoxin A (VacA)), and effector proteins (e.g., cytotoxin-associated gene A (CagA)) involved in colonisation, immune evasion, and disease induction. H. pylori not only cleverly evades the immune system but also robustly induces immune responses. This insidious bacterium employs various strategies to evade human innate and adaptive immune responses, leading to a life-long infection. Owing to the alteration of surface molecules, innate immune receptors couldn't recognise this bacterium; moreover, modulation of effector T cells subverts adaptive immune response. Most of the infected humans are asymptomatic and only a few of them present severe clinical outcomes. Therefore, the identification of virulence factors will pave the way for the prediction of infection severity and the development of an effective vaccine. H. pylori virulence factors are hereby comprehensively reviewed and the bacterium evasion from the immune response is properly discussed.

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Section: The Genome and Virulence Factors Of H Pylorimentioning

confidence: 99%

Section: The Genome and Virulence Factors Of H Pylorimentioning

confidence: 99%

Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

Mohammadzadeh,

Menbari,

Pishdadian

et al. 2023

Expert Rev. Mol. Med.

View full text Add to dashboard Cite

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“…Peptic ulcers consist of gastric ulcers (accounting for one-third of peptic ulcers) and duodenal ulcers (accounting for the rest) (Hopkins et al, 1996). H. pylori produces deleterious enzymes such as proteases, including serine protease high temperature requirement A (HtrA), collagenase Hp0169, catalase, urease, lipases, phospholipases, the cell-translocating serine/threonine kinase (CtkA) and some other potent ulcerogens, as well as platelet activating factor (PAF) and LTB4 (leukotriene B4) (Denizot et al, 1990;Fukuda et al, 1990;Sidebotham et al, 1991;Wessler, 2016). Lu et al (2005) showed that dupA is found in 42% of patients with duodenal ulcer.…”

Section: Peptic Ulcers Caused By H Pylorimentioning

confidence: 99%

Propolis: The future therapy against Helicobacter pylori-mediated gastrointestinal diseases

Shapla

Raihan

Islam

et al. 2018

JAB

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Helicobacter pylori (H. pylori), which is found in the stomach of approximately 50% of humans, remains there for almost the entire lifetime of the infected individual, leading to various gastrointestinal tractassociated disorders following full-blown infection. Due to the emergence of antibiotic resistance, recurrence and high cost of therapy, most antibiotic-based treatment strategies are not very effective in eradicating H. pylori infections. The quest for an alternative treatment free of these inconveniences is currently in demand. One of the important alternatives is propolis, produced by the honeybee Apis mellifera, which has been used to treat different diseases since it possesses a wide range of biochemical properties. Propolis has been reported as a useful therapeutic regimen against H. pylori, which is an important cause of gastric inflammation, peptic ulcer, gastric cancer, and lymphomas of mucosaassociated lymphoid tissues. Apart from propolis, various active compounds of other natural products have also been confirmed to be effective. This review compiles the scientific evidence of the role of propolis and other natural products against H. pylori-associated gastrointestinal tract-related health complexities by acing as an anti-angiogenic, anti-inflammatory, and antioxidant factor as well as via modulation of enzymatic activities.

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Emerging Novel Virulence Factors of Helicobacter pylori

Cited by 2 publications

References 118 publications

Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

Propolis: The future therapy against Helicobacter pylori-mediated gastrointestinal diseases

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