scholarly journals Erratum to: Prevalence and distribution of Helicobacter pylori cagA and vacA genotypes in the Moroccan population with gastric disease

2013 ◽  
Vol 32 (7) ◽  
pp. 969-969 ◽  
Author(s):  
S. Alaoui Boukhris ◽  
D.-a. Benajah ◽  
K. Rhazi ◽  
S. A. Ibrahimi ◽  
C. Nejjari ◽  
...  
2011 ◽  
Vol 31 (8) ◽  
pp. 1775-1781 ◽  
Author(s):  
S. A. Boukhris ◽  
D.-a. Benajah ◽  
K. Rhazi ◽  
S. A. Ibrahimi ◽  
C. Nejjari ◽  
...  

Author(s):  
Mounia El Khadir ◽  
Samia Alaoui Boukhris ◽  
Souad Oirdi Zahir ◽  
Dafr-ALLAH. Benajah ◽  
Sidi Adil Ibrahimi ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0170616 ◽  
Author(s):  
Mounia El Khadir ◽  
Samia Alaoui Boukhris ◽  
Dafr-Allah Benajah ◽  
Karima El Rhazi ◽  
Sidi Adil Ibrahimi ◽  
...  

2016 ◽  
Vol 29 (7-8) ◽  
pp. 476 ◽  
Author(s):  
Elisabete Coelho ◽  
Ana Magalhães ◽  
Mário Dinis-Ribeiro ◽  
Celso A. Reis

Introduction: Helicobacter pylori infection is very prevalent worldwide and is associated with the progression of the gastriccarcinogenesis cascade, being one of the main risk factors for the development of gastric carcinoma. Several factors are determinant for the infection and for the development of gastric disease, including environmental factors, host genetic factors and virulence factors of the bacteria.Material and Methods: In this review, we present an overview of the current knowledge on the determinants of the infection and on the recently described molecular mechanisms of Helicobacter pylori adhesion to the gastric mucosa, as well as its possible future therapeutic application.Results: The adhesion of Helicobacter pylori to the gastric epithelium is critical for gastric pathogenesis, allowing bacterial access to nutrients and the action of bacterial virulence factors, promoting recurrence of the infection and the progression of the gastric carcinogenesis pathway.Discussion: Eradication of Helicobacter pylori infection is the best preventive strategy available against gastric cancer, mainly if it is achieved before the development of pre-neoplastic lesions. The increase in antibiotics resistance, together with the eradication failures in some patients, has promoted the development of alternative treatments.Conclusion: The new therapeutic strategies, focused on the molecular mechanism of Helicobacter pylori adhesion, are very promising; however, future studies are needed to evaluate its in vivo efficiency and toxicity.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Pia Palamides ◽  
Tolulope Jolaiya ◽  
Ayodeji Idowu ◽  
Eva Loell ◽  
Charles Onyekwere ◽  
...  

2009 ◽  
Vol 191 (23) ◽  
pp. 7343-7352 ◽  
Author(s):  
Delia M. Pinto-Santini ◽  
Nina R. Salama

ABSTRACT Helicobacter pylori strains harboring the cag pathogenicity island (PAI) have been associated with more severe gastric disease in infected humans. The cag PAI encodes a type IV secretion (T4S) system required for CagA translocation into host cells as well as induction of proinflammatory cytokines, such as interleukin-8 (IL-8). cag PAI genes sharing sequence similarity with T4S components from other bacteria are essential for Cag T4S function. Other cag PAI-encoded genes are also essential for Cag T4S, but lack of sequence-based or structural similarity with genes in existing databases has precluded a functional assignment for the encoded proteins. We have studied the role of one such protein, Cag3 (HP0522), in Cag T4S and determined Cag3 subcellular localization and protein interactions. Cag3 is membrane associated and copurifies with predicted inner and outer membrane Cag T4S components that are essential for Cag T4S as well as putative accessory factors. Coimmunoprecipitation and cross-linking experiments revealed specific interactions with HpVirB7 and CagM, suggesting Cag3 is a new component of the Cag T4S outer membrane subcomplex. Finally, lack of Cag3 lowers HpVirB7 steady-state levels, further indicating Cag3 makes a subcomplex with this protein.


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