scholarly journals Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity

Toxins ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 677 ◽  
Author(s):  
Shamshul Ansari ◽  
Yoshio Yamaoka
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Bacterial Colonization ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Bacterial Virulence ◽  
Effector Proteins ◽  
Host Genetic ◽  
Colonization Factors ◽  
H Pylori

Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.

scholarly journals Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Extracellular Vesicles ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Infected Cells ◽  
H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

scholarly journals Carbonic Anhydrases: New Perspectives on Protein Functional Role and Inhibition in Helicobacter pylori

2021 ◽  
Vol 12 ◽  
Author(s):  
Cristina Campestre ◽  
Viviana De Luca ◽  
Simone Carradori ◽  
Rossella Grande ◽  
Vincenzo Carginale ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Pathogenic Bacteria ◽  
Acid Tolerance ◽  
Membrane Vesicles ◽  
Research Field ◽  
Outer Membrane Vesicles ◽  
Bacterial Toxin ◽  
Carbonic Anhydrases ◽  
Ph Homeostasis ◽  
H Pylori

Our understanding of the function of bacterial carbonic anhydrases (CAs, EC 4.2.1.1) has increased significantly in the last years. CAs are metalloenzymes able to modulate CO2, HCO3– and H+ concentration through their crucial role in catalysis of reversible CO2 hydration (CO2 + H2O ⇄ HCO3– + H+). In all living organisms, CA activity is linked to physiological processes, such as those related to the transport and supply of CO2 or HCO3–, pH homeostasis, secretion of electrolytes, biosynthetic processes and photosynthesis. These important processes cannot be ensured by the very low rate of the non-catalyzed reaction of CO2 hydration. It has been recently shown that CAs are important biomolecules for many bacteria involved in human infections, such as Vibrio cholerae, Brucella suis, Salmonella enterica, Pseudomonas aeruginosa, and Helicobacter pylori. In these species, CA activity promotes microorganism growth and adaptation in the host, or modulates bacterial toxin production and virulence. In this review, recent literature in this research field and some of the above-mentioned issues are discussed, namely: (i) the implication of CAs from bacterial pathogens in determining the microorganism growth and virulence; (ii) the druggability of these enzymes using classical CA inhibitors (CAIs) of the sulfonamide-type as examples; (iii) the role played by Helicobacter pylori CAs in the acid tolerance/adaptation of the microbe within the human abdomen; (iv) the role of CAs played in the outer membrane vesicles spawned by H. pylori in its planktonic and biofilm phenotypes; (v) the possibility of using H. pylori CAIs in combination with probiotic strains as a novel anti-ulcer treatment approach. The latter approach may represent an innovative and successful strategy to fight gastric infections in the era of increasing resistance of pathogenic bacteria to classical antibiotics.

scholarly journals Multiple in vivo passages enhance the ability of a clinical Helicobacter pylori isolate to colonize the stomach of Mongolian gerbils and to induce gastritis

2005 ◽  
Vol 39 (2) ◽  
pp. 221-229 ◽  
Author(s):  
A Bleich ◽  
I Köhn ◽  
S Glage ◽  
W Beil ◽  
S Wagner ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Bacterial Colonization ◽  
Underlying Mechanism ◽  
Mongolian Gerbils ◽  
Histopathological Changes ◽  
Genetic Changes ◽  
Colonization Ability ◽  
Colonization Factors ◽  
H Pylori

The Mongolian gerbil is an excellent animal model for Helicobacter pylori-induced gastritis in humans. In this study, initially low colonization rates of the H. pylori strains ATCC 43504, SS1, or HP87 inoculated into gerbils caused difficulties in establishing this model. In order to increase the colonization ability and pathogenicity, the clinical HP87 isolate was selected for adaptation to the gerbil stomach by multiple in vivo passages through gerbils. Development of gastritis was examined histologically at 4–52 weeks after infection. The proportion of gerbils which tested positive for H. pylori by culture at four weeks after inoculation gradually increased from 11.1% of gerbils inoculated with HP87 without prior in vivo passage (P0) to 100% of gerbils inoculated with HP87 with seven in vivo passages (P7). In addition, adaptation of HP87 resulted in more severe histopathological changes. Gerbils infected with adapted HP87 (P7) exhibited severe infiltration by monomorphonuclear and polymorphonuclear leukocytes in the mucosa, submucosa, and subserosa of the gastric antrum, as well as epithelial changes consisting of hyperplasia, erosion, and ulceration. Histopathological changes increased in severity from four to 52 weeks after infection. Adaptation of HP87 during its passages through gerbils could be due to genetic changes in bacterial colonization factors. Identification of these changes might be useful to understand the underlying mechanism of gastric adaptation and pathogenesis of H. pylori.

A review of the possible bacterial determinants of clinical outcome inHelicobacter pyloriinfection

1998 ◽  
Vol 44 (3) ◽  
pp. 201-210 ◽  
Author(s):  
Carlo A Fallone ◽  
Alan N Barkun ◽  
Markus U Göttke ◽  
Robin N Beech
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Outcome ◽  
Virulence Factors ◽  
Bacterial Virulence ◽  
Disease Outcome ◽  
Future Research ◽  
Susceptible Host ◽  
Ulcer Disease ◽  
Increased Risk ◽  
H Pylori

Helicobacter pylori is present in 40-60% of the population and approximately 10-20% of these infected individuals suffer from a H. pylori associated disease such as peptic ulcer disease or gastric cancer. This article reviews the potential bacterial determinants responsible for and markers predictive of both the acquisition of H. pylori infection and subsequent clinical outcome; i.e., asymptomatic infection or disease. The acquisition of H. pylori infection depends on exposure (hence the increased risk in lower socioeconomic groups and developing nations) to viable bacteria with at least a functional urease gene in a susceptible host. Once infection occurs, bacterial virulence factors, including the vacuolating cytotoxin, and genes of the cag pathogenicity island, as well as nonbacterial factors may determine disease outcome. Future research is being directed at discovering other bacterial virulence factors responsible for the different clinical outcomes of H. pylori infection. This will be greatly enhanced by the recent release of the complete genome sequence of H. pylori. The determination of the relative importance of each of these recognized and other as yet unrecognized factors responsible for disease outcome will assist in the appropriate targeting of patients in the treatment of H. pylori infection.Key words: Helicobacter pylori, genetics, virulence, bacterial.

scholarly journals Long-Distance Delivery of Bacterial Virulence Factors by Pseudomonas aeruginosa Outer Membrane Vesicles

2009 ◽  
Vol 5 (4) ◽  
pp. e1000382 ◽  
Author(s):  
Jennifer M. Bomberger ◽  
Daniel P. MacEachran ◽  
Bonita A. Coutermarsh ◽  
Siying Ye ◽  
George A. O'Toole ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Outer Membrane ◽  
Virulence Factors ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Bacterial Virulence ◽  
Long Distance ◽  
Distance Delivery

scholarly journals Outer Membrane Vesicles Secreted by Helicobacter pylori Transmitting Gastric Pathogenic Virulence Factors

ACS Omega ◽  
2021 ◽  
Author(s):  
Sisi Wei ◽  
Xiaoya Li ◽  
Jingjing Wang ◽  
Yaojie Wang ◽  
Cong Zhang ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Virulence Factors ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles

scholarly journals Selective Inhibition of Helicobacter pylori Carbonic Anhydrases by Carvacrol and Thymol Could Impair Biofilm Production and the Release of Outer Membrane Vesicles

2021 ◽  
Vol 22 (21) ◽  
pp. 11583
Author(s):  
Rossella Grande ◽  
Simone Carradori ◽  
Valentina Puca ◽  
Irene Vitale ◽  
Andrea Angeli ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Bacterial Resistance ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Peptic Ulcers ◽  
Carbonic Anhydrases ◽  
Biofilm Production ◽  
Isoform Selectivity ◽  
H Pylori

Helicobacter pylori, a Gram-negative neutrophilic pathogen, is the cause of chronic gastritis, peptic ulcers, and gastric cancer in humans. Current therapeutic regimens suffer from an emerging bacterial resistance rate and poor patience compliance. To improve the discovery of compounds targeting bacterial alternative enzymes or essential pathways such as carbonic anhydrases (CAs), we assessed the anti-H. pylori activity of thymol and carvacrol in terms of CA inhibition, isoform selectivity, growth impairment, biofilm production, and release of associated outer membrane vesicles-eDNA. The microbiological results were correlated by the evaluation in vitro of H. pylori CA inhibition, in silico analysis of the structural requirements to display such isoform selectivity, and the assessment of their limited toxicity against three probiotic species with respect to amoxicillin. Carvacrol and thymol could thus be considered as new lead compounds as alternative H. pylori CA inhibitors or to be used in association with current drugs for the management of H. pylori infection and limiting the spread of antibiotic resistance.

scholarly journals Concurrent detection of cagA, vacA, sodB and hsp60 virulence genes and their relationship with clinical outcomes of disease in Helicobacter pylori isolated strains of southwest of Iran

2019 ◽  
Author(s):  
Mansour Amin ◽  
Ali Akbar Shayesteh ◽  
Amirarsalan Serajian
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Statistical Tests ◽  
Agar Plate ◽  
Polymyxin B ◽  
Bacterial Virulence ◽  
The Difference ◽  
H Pylori ◽  
Southwest Of Iran

Background and Objectives: Helicobacter pylori is a Gram-negative spiral-shaped bacterium that contaminates more than half of the world's inhabitants, and infection with this bacterium is associated with some gastric disorders. Also, 5% to 10% of H. pylori genes are specific to this bacterium and many bacterial virulence factors fall into this group. The cagA, vacA, sodB and hsp60 are among important virulence factors of H. pylori. Materials and Methods: A gastric biopsy specimen was taken from 341 gastric patients and cultivated on a Colombia agar plate, containing various antibiotics, such as vancomycin, amphotericin B, and trimethoprim & polymyxin B, and incubated for 3 to 10 days under microaerophilic conditions at 37°C. PCR was used to detect the ureC, cagA, vacA, sodB and hsp60 genes. Results: In this study, 131 isolates were identified as H. pylori. The prevalence of cagA, vacA, sodB and hsp60 were 74%, 100%, 92.4% and 96.2%, respectively. The correlation between the clinical forms of the disease and the virulence genes were analyzed by statistical tests and no significant correlation was found. Conclusion: The obtained results are similar to some studies conducted in different parts of the world and is different in other cases. This discrepancy is due to the difference in the type of gastric disorders, sample size and methodology.

scholarly journals Expression of Helicobacter pylori Virulence Factors and Associated Expression Profiles of Inflammatory Genes in the Human Gastric Mucosa

2007 ◽  
Vol 75 (11) ◽  
pp. 5118-5126 ◽  
Author(s):  
Sicheng Wen ◽  
Dominique Velin ◽  
Christian P. Felley ◽  
Likun Du ◽  
Pierre Michetti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Virulence Factors ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Bacterial Colonization ◽  
Expression Patterns ◽  
Human Gastric Mucosa ◽  
H Pylori

ABSTRACT Helicobacter pylori virulence factors have been suggested to be important in determining the outcome of infection. The H. pylori adhesion protein BabA2 is thought to play a crucial role in bacterial colonization and in induction of severe gastric inflammation, particularly in combination with expression of CagA and VacA. However, the influence of these virulence factors on the pathogenesis of H. pylori infection is still poorly understood. To address this question, the inflammatory gene expression profiles for two groups of patients infected with triple-negative strains (lacking expression of cagA, babA2, and vacAs1 but expressing vacAs2) and triple-positive strains (expressing cagA, vacAs1, and babA2 but lacking expression of vacAs2) were investigated. The gene expression patterns in the antrum gastric mucosa from patients infected with different H. pylori strains were very similar, and no differentially expressed genes could be identified by pairwise comparisons. Our data thus suggest that there is a lack of correlation between the host inflammatory responses in the gastric mucosa and expression of the babA2, cagA, and vacAs1 genes.

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