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 Virulence Factors of Helicobacter pylori: A Review

2014 ◽  
Vol 7 ◽  
pp. CGast.S13760 ◽  
Author(s):  
Bruna M. Roesler ◽  
Elizabeth M.A. Rabelo-Gonçalves ◽  
José M.R. Zeitune
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Outcome ◽  
Virulence Factors ◽  
Ulcer Disease ◽  
Clinical Disorders ◽  
H Pylori ◽  
High Level ◽  
Upper Gastrointestinal ◽  
Host Characteristics

Helicobacter pylori is a spiral-shaped Gram-negative bacterium that colonizes the human stomach and can establish a long-term infection of the gastric mucosa, a condition that affects the relative risk of developing various clinical disorders of the upper gastrointestinal tract, such as chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma. H. pylori presents a high-level of genetic diversity, which can be an important factor in its adaptation to the host stomach and also for the clinical outcome of infection. There are important H. pylori virulence factors that, along with host characteristics and the external environment, have been associated with the different occurrences of diseases. This review is aimed to analyzing and summarizing the main of them and possible associations with the clinical outcome.

scholarly journals The Role of Interleukin-1Beta and Other Potential Genetic Markers as Indicators of Gastric Cancer Risk

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 8B-12B ◽  
Author(s):  
Esther Troost ◽  
Georgina L Hold ◽  
Malcolm G Smith ◽  
Wong-Ho Chow ◽  
Charles S Rbkin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Clinical Outcome ◽  
Genetic Factors ◽  
Interleukin 1 ◽  
Subsequent Development ◽  
Ulcer Disease ◽  
Increased Risk ◽  
Host Genetic ◽  
H Pylori ◽  
Host Genetic Factors

Helicobacter pyloriinfects half of the world’s population, and is associated with asymptomatic gastritis and also with more serious conditions such as peptic ulcer disease and gastric carcinoma. The clinical outcome is largely dependent on the severity and distribution of theH pylori-induced gastritis, but the pathogenesis remains poorly understood. Bacterial virulence factors and environmental influences contribute to the pathogenesis, but do not explain the divergent outcomes. There is emerging evidence that host genetic factors play a key role in determining the clinical outcome ofH pyloriinfection. In particular, proinflammatory genotypes of the interleukin-1 beta (IL-1β) gene are associated with an increased risk of gastric cancer and its precursors. The effects are most likely mediated through the induction of hypochlorhydria and severe corpus gastritis with the subsequent development of gastric atrophy. The roles of IL-1β and other host genetic factors in the pathogenesis ofH pylorirelated cancer are discussed in this article.

scholarly journals Relationship of interleukin-1B gene promoter region polymorphism with Helicobacter pylori infection and gastritis

2015 ◽  
Vol 9 (10) ◽  
pp. 1108-1116 ◽  
Author(s):  
Ivy Bastos Ramis ◽  
Júlia Silveira Vianna ◽  
Priscila Cristina Bartolomeu Halicki ◽  
Caroline Lara ◽  
Thássia Fernanda Tadiotto ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Promoter Region ◽  
Gene Promoter ◽  
Helicobacter Pylori Infection ◽  
Caga Gene ◽  
Gastric Diseases ◽  
Ulcer Disease ◽  
Increased Risk ◽  
H Pylori ◽  
Relationship Of

Introduction: Helicobacter pylori infection is associated with gastritis, peptic ulcer disease and gastric carcinoma. The severity of damage is determined by the interplay between environmental/behavioral factors, bacterial pathogenicity genes and host genetic polymorphisms that can influence the secretion levels of inflammatory cytokines. Accordingly, this study aimed to identify polymorphisms in the IL-1B and IL-1RN genes and their associations with H. pylori infection, cagA gene of H. pylori, and gastroduodenal diseases. Methodology: Gastric biopsy samples from 151 patients infected with H. pylori and 76 uninfected individuals were analyzed. H. pylori infection was diagnosed by histology and PCR. Polymorphisms at positions -511, -31 and +3954 of the IL-1B gene were detected by PCR-RFLP, and an analysis of the VNTR polymorphism of the IL-1RN gene was performed by PCR. Results: It was observed that the presence of the T/T genotype at position -511 and the C/C genotype at position -31 were associated with H. pylori infection and with an increased risk of gastritis in H. pylori-positive patients. Additionally, strains from patients H. pylori-positive carrying the cagA gene was significantly related with the T/T genotype at position -511 of IL-1B.  No association of polymorphisms at position +3954 of IL-1B and in the IL-1RN with H. pylori infection and with risk of severe gastric diseases was found. Conclusions: We demonstrated that polymorphisms in the promoter region of the IL-1B gene (at positions -511 and -31) are associated with an enhanced risk of H. pylori infection as well as gastritis in H. pylori-positive patients.

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.

Immune responses to Helicobacter pylori colonization: mechanisms and clinical outcomes

2006 ◽  
Vol 110 (3) ◽  
pp. 305-314 ◽  
Author(s):  
Cynthia Portal-Celhay ◽  
Guillermo I. Perez-Perez
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Immune Responses ◽  
Gastric Lymphoma ◽  
Gastric Epithelium ◽  
Immune Effector ◽  
Ulcer Disease ◽  
Gastroduodenal Disease ◽  
Increased Risk ◽  
H Pylori

Helicobacter pylori colonizes the stomachs of half of the world's population and usually persists in the gastric mucosa of human hosts for decades or life. Although most H. pylori-positive people are asymptomatic, the presence of H. pylori is associated with increased risk for the development of peptic ulcer disease, gastric adenocarcinoma and gastric lymphoma. The development of a sustained gastric inflammatory and immune response to infection appears to be pivotal for the development of disease. During its long co-existence with humans, H. pylori has evolved complex strategies to maintain a mild inflammation of the gastric epithelium while limiting the extent of immune effector activity. In this review, the nature of the host immune response to H. pylori infection and the mechanism employed by the bacterium to evade them is considered. Understanding the mechanisms of colonization, persistence and virulence factors of the bacterium as well as the innate and adaptive immune responses of the host are critically important for the development of new strategies to prevent the development of H. pylori-induced gastroduodenal disease.

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 Detection of Anti-VacA Antibody Responses in Serum and Gastric Juice Samples Using Type s1/m1 and s2/m2 Helicobacter pylori VacA Antigens

1999 ◽  
Vol 6 (4) ◽  
pp. 489-493 ◽  
Author(s):  
Guillermo I. Perez-Perez ◽  
Richard M. Peek ◽  
John C. Atherton ◽  
Martin J. Blaser ◽  
Timothy L. Cover
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Juice ◽  
Antibody Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serum Samples ◽  
Ulcer Disease ◽  
Serum Igg ◽  
Increased Risk ◽  
Antigenic Properties ◽  
H Pylori

ABSTRACT Several different families of vacuolating toxin (vacA) alleles are present in Helicobacter pylori, and they encode products with differing functional activities. H. pyloristrains containing certain types of vacA alleles have been associated with an increased risk for peptic ulcer disease. In this study, we tested serum samples and gastric juice from 19 H. pylori-negative and 39 H. pylori-positive patients for enzyme-linked immunosorbent assay reactivity with two different types of VacA antigens (types s1/m1 and s2/m2), which were purified from H. pylori 60190 and 86-338, respectively. Both antigens were recognized better by serum immunoglobulin G (IgG) fromH. pylori-positive persons than by serum IgG from H. pylori-negative persons (P < 0.01). The s1/m1 VacA antigen was better recognized by sera from patients carryingvacA type s1/m1 strains than by sera from patients carryingvacA type s2/m2 or s1/m2 strains (P < 0.01). Conversely, the s2/m2 VacA antigen was better recognized by sera from patients carrying type s2/m2 or s1/m2 strains (P= 0.03). Serum IgG anti-VacA antibodies were present more frequently in patients carrying type s1/m1 strains than in other H. pylori-positive patients (P = 0.0002). In addition, the highest levels of IgA anti-VacA antibodies were detected in the gastric juice of patients carrying type s1/m1 strains. These data indicate that different VacA isoforms have distinct antigenic properties and that multiple forms of VacA elicit antibody responses inH. pylori-positive humans.

scholarly journals High Prevalence of Helicobacter pylori Infection, Atrophic Gastritis and Hypochlorhydria in HIV-Positive Cameroonians Tested by Serological Stomach-Specific Biomarkers (GastroPanel®)

2021 ◽  
pp. 40-48
Author(s):  
Alonge Ivo Ebule ◽  
Valentine Ngum Ndze ◽  
Ngouana Kammalac Thierry ◽  
Lebongo Belayang Marie ◽  
Mbopiwou Nforen Ismaila ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Demographic Data ◽  
Significant Risk ◽  
Cd4 Counts ◽  
Ulcer Disease ◽  
Software Application ◽  
Increased Risk ◽  
H Pylori ◽  
Hiv Aids

Background: The human immunodeficiency virus (HIV) and Helicobacter pylori (H. pylori) are associated with significant chronic inflammation of the gastric mucosa. Gastric inflammation is a precursor to many gastrointestinal disorders including, peptic ulcer disease, atrophic gastritis (AG) and gastric cancer (GC). AG is usually accompanied by low hydrochloric acid (hypochlorhydria), low pepsinogens (PG) and high gastrin (G) levels and is the most significant risk condition for GC. Acid-free stomach is a risk factor for impaired drug absorption including anti-retroviral therapy and antibiotics. The role of H. pylori infection in HIV-infected subjects has been conflicting. Objectives: We assessed the prevalence of H. pylori infection, AG and acid-free stomach (hypochlorhydria) amongst HIV/AIDS subjects in Yaounde Cameroon. Methods: HIV/AIDS subjects were recruited during January-May 2018. Clinical and socio-demographic data of the subjects were recorded. An aliquot of 5 ml of blood was aseptically collected for analysis by GastroPanel® biomarker test for PGI, PGII, G-17 and H.pylori IgG antibodies. GastroPanel results were interpreted using the software application GastroSoft®. Statistical analyses were run by Epiinfo7.0. Ethical clearance was obtained from the National Ethics Committee. Results: A total of 84 subjects were recruited, aged between 17-63 years (mean 37.6 ± 8.9 years). H. pylori seropositivity (IgG ≥30 EIU) was detected in 68(81.0%) of the subjects. H. pylori seropositivity was closely associated with low CD4 counts (p=0.01). Altogether, 26(31.0%) of the subjects presented with AG of the corpus while, hypochlorhydria was detected in 32(38.1%) of the patients. AG and hypochlorhydria were associated with low CD4 counts<200μl/l (p=0.01) and (p=0.005), respectively. Conclusion: H. pylori infection, AG and acid-free stomach were common among HIV/AIDS patients, associated with an increased risk for GC and impaired absorption of micronutrients and some medicines.

scholarly journals Riboregulation in the Major Gastric Pathogen Helicobacter pylori

2021 ◽  
Vol 12 ◽  
Author(s):  
Alejandro Tejada-Arranz ◽  
Hilde De Reuse
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Antisense Rna ◽  
Small Rnas ◽  
Genetic Regulation ◽  
Type I ◽  
Control Of Gene Expression ◽  
Ulcer Disease ◽  
Interesting Study ◽  
H Pylori

Helicobacter pylori is a Gram-negative bacterial pathogen that colonizes the stomach of about half of the human population worldwide. Infection by H. pylori is generally acquired during childhood and this bacterium rapidly establishes a persistent colonization. H. pylori causes chronic gastritis that, in some cases, progresses into peptic ulcer disease or adenocarcinoma that is responsible for about 800,000 deaths in the world every year. H. pylori has evolved efficient adaptive strategies to colonize the stomach, a particularly hostile acidic environment. Few transcriptional regulators are encoded by the small H. pylori genome and post-transcriptional regulation has been proposed as a major level of control of gene expression in this pathogen. The transcriptome and transcription start sites (TSSs) of H. pylori strain 26695 have been defined at the genome level. This revealed the existence of a total of 1,907 TSSs among which more than 900 TSSs for non-coding RNAs (ncRNAs) including 60 validated small RNAs (sRNAs) and abundant anti-sense RNAs, few of which have been experimentally validated. An RNA degradosome was shown to play a central role in the control of mRNA and antisense RNA decay in H. pylori. Riboregulation, genetic regulation by RNA, has also been revealed and depends both on antisense RNAs and small RNAs. Known examples will be presented in this review. Antisense RNA regulation was reported for some virulence factors and for several type I toxin antitoxin systems, one of which controls the morphological transition of H. pylori spiral shape to round coccoids. Interestingly, the few documented cases of small RNA-based regulation suggest that their mechanisms do not follow the same rules that were well established in the model organism Escherichia coli. First, the genome of H. pylori encodes none of the two well-described RNA chaperones, Hfq and ProQ that are important for riboregulation in several organisms. Second, some of the reported small RNAs target, through “rheostat”-like mechanisms, repeat-rich stretches in the 5′-untranslated region of genes encoding important virulence factors. In conclusion, there are still many unanswered questions about the extent and underlying mechanisms of riboregulation in H. pylori but recent publications highlighted original mechanisms making this important pathogen an interesting study model.

scholarly journals Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 27
Author(s):  
Jacek Baj ◽  
Alicja Forma ◽  
Monika Sitarz ◽  
Piero Portincasa ◽  
Gabriella Garruti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Virulence Factors ◽  
Premalignant Lesions ◽  
Bacterial Pathogenicity ◽  
Current State ◽  
Genetic And Environmental Factors ◽  
H Pylori ◽  
Stimulation Of

Gastric cancer constitutes one of the most prevalent malignancies in both sexes; it is currently the fourth major cause of cancer-related deaths worldwide. The pathogenesis of gastric cancer is associated with the interaction between genetic and environmental factors, among which infection by Helicobacter pylori (H. pylori) is of major importance. The invasion, survival, colonization, and stimulation of further inflammation within the gastric mucosa are possible due to several evasive mechanisms induced by the virulence factors that are expressed by the bacterium. The knowledge concerning the mechanisms of H. pylori pathogenicity is crucial to ameliorate eradication strategies preventing the possible induction of carcinogenesis. This review highlights the current state of knowledge and the most recent findings regarding H. pylori virulence factors and their relationship with gastric premalignant lesions and further carcinogenesis.

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