scholarly journals Diseases of the oral mucosa associated with Helicobacter pylori

Author(s):  
Svetlana V. Tarasenko ◽  
M. A. Stepanov ◽  
S. A. Kalinin ◽  
V. V. Morozova

This study analyzed the role of Helicobacter pylori in the development of lesions of the oral mucosa and explored the relationship between the prevalence and intensity of periodontal disease and the stage, duration, and severity of gastrointestinal diseases associated with H. pylori infection. The newly identified factors of H. pylori pathogenicity that participate in the development of lesions of the oral mucosa in case of a body infection were also determined.

2019 ◽  
Vol 77 (9) ◽  
Author(s):  
Narges Dastmalchi ◽  
Seyed Mahdi Banan Khojasteh ◽  
Mirsaed Miri Nargesi ◽  
Reza Safaralizadeh

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.


2019 ◽  
Vol 20 (1) ◽  
pp. 23-28
Author(s):  
Yunzhan Zhang ◽  
Danyan Li ◽  
Yunkai Dai ◽  
Ruliu Li ◽  
Yong Gao ◽  
...  

Background: Helicobacter pylori (H. pylori)-related gastric diseases are a series of gastric mucosal disorders associated with H. pylori infection. Gastric cancer (GC) is widely believed to evolve from gastritis and gastric ulcer. As an important adhesion molecule of epithelial cells, E-cadherin plays a key role in the development of gastric diseases. In this review, we aim to seek the characteristic of E-cadherin expression at different stages of gastric diseases. Methods: We searched plenty of databases for research literature about E-cadherin expression in H. pylori-related gastric diseases, and reviewed the relationship of E-cadherin and H. pylori, and the role of E-cadherin at different stages of gastric diseases. Results: H. pylori was shown to decrease E-cadherin expression by various ways in vitro, while most of clinical studies have not found the relationship between H. pylori and E-cadherin expression. It is defined that poor outcome of GC is related to loss expression of E-cadherin, but it is still unclear when qualitative change of E-cadherin expression in gastric mucosa emerges. Conclusion: Expression level of E-cadherin in gastric cells may be a consequence of injury factors and body’s selfrepairing ability. More studies on E-cadherin expression in gastric mucosa with precancerous lesions need to be performed, which may be potential and useful for early detection, prevention and treatment of GC.


2003 ◽  
Vol 17 (suppl b) ◽  
pp. 18B-20B ◽  
Author(s):  
Jia-Qing Huang ◽  
Richard H Hunt

The relationship betweenHelicobacter pyloriinfection and the risk of gastric cancer has been well established in the last decade. Four metaanalyses have found that the infection increases the risk of noncardia gastric cancer by 2- to 6-fold compared with noninfected control populations. However, the role ofcagAstrains ofH pyloriin relation to gastric cancer has not been evaluated systematically. We undertook a meta-analysis of epidemiological studies examining the relationship between infection withcagA-positive strains ofH pyloriand the risk of gastric cancer, and found that patients who are seropositive forcagAstrains ofH pyloriare at an increased risk for developing noncardia gastric cancer compared with those withH pyloriinfection alone. Therefore, searching forcagA-positive strains ofH pylorimay help identify populations at a greater risk for developing gastric cancer.


2020 ◽  
Author(s):  
Masoud Keikha ◽  
Mohsen Karbalaei

Abstract Background: Helicobacter pylori (H. pylori) is one of the most well-known risk factors for getting the gastric cancer disease. In recent studies, the relationship between its virulence factors, specially CagA (cytotoxin‐associated gene A) toxin and development into the gastrointestinal diseases is taken into consideration. According to review of literature, despite the presence of four motifs A, B, C, and D in CagA toxin, two motifs C and D are more associated with gastrointestinal complications in patients who are infected by H. pylori. Methods: In the present study, we researched about theses ambiguities using a comprehensive meta-analysis study. In this study, we assessed the information of 1762 Iranian patients for potential relationship between all genotypes of cagA gene and gastrointestinal diseases.Results: According to statistical analysis, the abundance of cagA genotypes AB, ABC, ABCC, ABCCC, and ABD in Iranian population is 5.52%, 80.18%, 22.81%, 2.76%, and 0% respectively. In addition, it was determined that there is a significant relationship between cagA genotypes ABCC and ABCCC on the one hand and cagA genotype ABCCC on the other hand with susceptibility to chronic gastritis and gastric cancer respectively.Conclusions: Overall, it can be concluded that the higher number of EPIYA-C copy numbers lead to the higher risk of gastric cancer. According to our results, it seems that the presence of EPIYA-ABCCC motif in strains of H. pylori should be considered as an appropriate marker in preventing the gastric cancer among the Iranian population.


2016 ◽  
Vol 5 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Lingling Zu

Abstract Helicobacter pylori is one of the most common pathogens among humans, and it is also closely related to stomach diseases. Spread of its diseases must be understood to properly control H. pylori. Oral H. pylori may also play an important role in the spread of the bacterium. This study provides an overview on the role of oral H. pylori in spread, diagnosis, and prevention of this organism. The present work also determines difficulties encountered in current studies and progress of research on the relationship between oral H. pylori and oral diseases.


2019 ◽  
Vol 77 (4) ◽  
Author(s):  
Narges Dastmalchi ◽  
Reza Safaralizadeh ◽  
Seyed Mahdi Banan Khojasteh

ABSTRACT Helicobacter pylori infection and H. pylori-related gastric inflammation can be considered as the most significant promoter of gastric cancer (GC). Recent investigations have evaluated the regulatory function of microRNAs (miRNAs) in H. pylori pathogenesis and H. pylori-related diseases, especially GC. The present study reviewed the correlation between miRNAs and H. pylori in gastrointestinal diseases. Furthermore, the current review highlighted the role of H. pylori pathogen and some H. pylori-related virulence factors in the deregulation of various miRNAs, especially oncogenic miRNAs (miRs) and their associated molecular pathways. Among the related studies, some have focused on the effects of H. pylori infection on regulatory networks of miRs, while others have highlighted the effects of alterations in the expression level of miRs in H. pylori-related diseases. The connectivity between miRNAs and H. pylori is regulated by various molecular pathways and different molecular targets of miRNAs.


2019 ◽  
Vol 20 (2) ◽  
pp. 137-145 ◽  
Author(s):  
Kashyapi Chakravarty ◽  
Smriti Gaur

Helicobacter pylori, a pathogenic bacterium, has been known to be the root cause of numerous gastrointestinal disorders. In patients showing symptoms of its infection, antibiotic therapy is a likely treatment. However, the high cost of antibiotic therapy, associated antibiotic resistance along with other adverse effects has led to the use of probiotics for Helicobacter pylori treatment. In recent times, probiotics have played an essential role as complementary prophylaxis for gastrointestinal diseases, thus minimizing antibiotics’ usage and their side effects. Probiotics are live microbial agents that exude beneficial effects on their hosts when administered in the proper dosage. The growth of the organism has been reported to be inhibited to a great extent by probiotics and research employing animal models has shown a significant reduction in H. pylori-associated gastric inflammation. In human clinical trials, it has been observed that treatment with probiotics alleviated gastritis symptoms caused by H. pylori and reduced colonization of the organism. As expected, complete eradication of H. pylori infection has not yet been reported by the administration of probiotics alone. Complement treatments using probiotics have shown to benefit infected individuals by decreasing the harmful effects of H. pylori eradication treatment using antibiotics. Long-term administration of probiotics might have favourable outcomes in H. pylori infection especially by decreasing the risk of development of diseases caused by increased levels of gastric inflammation. One such chronic condition is gastric ulcer which occurs due to considerable damage to the mucosal barrier by H. pylori colonization. This review provides a brief description of the promising role of probiotics as a complementary treatment to control H. pylori infection and consequently the management of various gastrointestinal disorders among populations with a special focus on gastric ulcer.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Jesús K. Yamamoto-Furusho ◽  
Gabriela Fonseca-Camarillo ◽  
Carlos A. Barrera-Ochoa ◽  
Janette Furuzawa-Carballeda

Background/Aims. Epidemiological evidence suggests a relationship between Helicobacter pylori infection with the development of autoimmune diseases. H. pylori elicit a chronic systemic inflammatory response with the secretion of proinflammatory cytokines. IL-10 is a regulatory cytokine that plays a central role in limiting host immune response to pathogen. Increased IL-10 levels were reported in H. pylori–infected gastric mucosa. The aim of this study was to explore the relationship between IL-10 systemic synthesis and H. pylori infection in patients with ulcerative colitis. Methods. Detection of H. pylori infection was performed by a 13C-urea breath test in 31 patients with UC. In each patient, a serum sample was drawn to measure IL-10 by the ELISA technique. Based on the primary breath test result, two groups were formed and serum IL-10 was measured. Results. Serological IL-10 levels in patients with UC and negative 13C-urea breath test was 10.28 pg/ml whereas in patients with UC and positive 13C-urea breath test was 5.5 pg/ml (P=0.035). IL-10 levels were higher in the inflammatory endoscopic and histological active groups which tested positive in the 13C-urea breath tests for H. pylori (P<0.05).Conclusions. The role of IL-10 secretion in patients with UC in determining the clinicopathological outcome of infection merits further study. This study suggests an association between serum IL-10 and disease severity in patients with UC and HP infection.


Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 331
Author(s):  
Montserrat Palau ◽  
Núria Piqué ◽  
M. José Ramírez-Lázaro ◽  
Sergio Lario ◽  
Xavier Calvet ◽  
...  

Helicobacter pylori is a common pathogen associated with several severe digestive diseases. Although multiple virulence factors have been described, it is still unclear the role of virulence factors on H. pylori pathogenesis and disease progression. Whole genome sequencing could help to find genetic markers of virulence strains. In this work, we analyzed three complete genomes from isolates obtained at the same point in time from a stomach of a patient with adenocarcinoma, using multiple available bioinformatics tools. The genome analysis of the strains B508A-S1, B508A-T2A and B508A-T4 revealed that they were cagA, babA and sabB/hopO negative. The differences among the three genomes were mainly related to outer membrane proteins, methylases, restriction modification systems and flagellar biosynthesis proteins. The strain B508A-T2A was the only one presenting the genotype vacA s1, and had the most distinct genome as it exhibited fewer shared genes, higher number of unique genes, and more polymorphisms were found in this genome. With all the accumulated information, no significant differences were found among the isolates regarding virulence and origin of the isolates. Nevertheless, some B508A-T2A genome characteristics could be linked to the pathogenicity of H. pylori.


mBio ◽  
2014 ◽  
Vol 5 (4) ◽  
Author(s):  
Adria Carbo ◽  
Danyvid Olivares-Villagómez ◽  
Raquel Hontecillas ◽  
Josep Bassaganya-Riera ◽  
Rupesh Chaturvedi ◽  
...  

ABSTRACTThe development of gastritis duringHelicobacter pyloriinfection is dependent on an activated adaptive immune response orchestrated by T helper (Th) cells. However, the relative contributions of the Th1 and Th17 subsets to gastritis and control of infection are still under investigation. To investigate the role of interleukin-21 (IL-21) in the gastric mucosa duringH. pyloriinfection, we combined mathematical modeling of CD4+T cell differentiation within vivomechanistic studies. We infected IL-21-deficient and wild-type mice withH. pyloristrain SS1 and assessed colonization, gastric inflammation, cellular infiltration, and cytokine profiles. ChronicallyH. pylori-infected IL-21-deficient mice had higherH. pyloricolonization, significantly less gastritis, and reduced expression of proinflammatory cytokines and chemokines compared to these parameters in infected wild-type littermates. Thesein vivodata were used to calibrate anH. pyloriinfection-dependent, CD4+T cell-specific computational model, which then described the mechanism by which IL-21 activates the production of interferon gamma (IFN-γ) and IL-17 during chronicH. pyloriinfection. The model predicted activated expression of T-bet and RORγt and the phosphorylation of STAT3 and STAT1 and suggested a potential role of IL-21 in the modulation of IL-10. Driven by our modeling-derived predictions, we found reduced levels of CD4+splenocyte-specifictbx21androrcexpression, reduced phosphorylation of STAT1 and STAT3, and an increase in CD4+T cell-specific IL-10 expression inH. pylori-infected IL-21-deficient mice. Our results indicate that IL-21 regulates Th1 and Th17 effector responses during chronicH. pyloriinfection in a STAT1- and STAT3-dependent manner, therefore playing a major role controllingH. pyloriinfection and gastritis.IMPORTANCEHelicobacter pyloriis the dominant member of the gastric microbiota in more than 50% of the world’s population.H. pyloricolonization has been implicated in gastritis and gastric cancer, as infection withH. pyloriis the single most common risk factor for gastric cancer. Current data suggest that, in addition to bacterial virulence factors, the magnitude and types of immune responses influence the outcome of colonization and chronic infection. This study uses a combined computational and experimental approach to investigate how IL-21, a proinflammatory T cell-derived cytokine, maintains the chronic proinflammatory T cell immune response driving chronic gastritis duringH. pyloriinfection. This research will also provide insight into a myriad of other infectious and immune disorders in which IL-21 is increasingly recognized to play a central role. The use of IL-21-related therapies may provide treatment options for individuals chronically colonized withH. pylorias an alternative to aggressive antibiotics.


Sign in / Sign up

Export Citation Format

Share Document