Journal articles: 'Human Pathogen Helicobacter'

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Forbes, GeoffreyM, BrendanJ Collins, Adam Harris, J. J. Misiewicz, Liam Murray, and Ian Harvey. "Helicobacter pylori: a human pathogen." Lancet 345, no. 8964 (June 1995): 1579–80. http://dx.doi.org/10.1016/s0140-6736(95)91132-4.

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Graham, J. R. "Helicobacter pylori: human pathogen or simply an opportunist?" Lancet 345, no. 8957 (April 1995): 1095–97. http://dx.doi.org/10.1016/s0140-6736(95)90824-2.

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Haley, Kathryn P., and Jennifer A. Gaddy. "Helicobacter pylori: Genomic Insight into the Host-Pathogen Interaction." International Journal of Genomics 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/386905.

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The advent of genomic analyses has revolutionized the study of human health. Infectious disease research in particular has experienced an explosion of bacterial genomic, transcriptomic, and proteomic data complementing the phenotypic methods employed in traditional bacteriology. Together, these techniques have revealed novel virulence determinants in numerous pathogens and have provided information for potential chemotherapeutics. The bacterial pathogen,Helicobacter pylori, has been recognized as a class 1 carcinogen and contributes to chronic inflammation within the gastric niche. Genomic analyses have uncovered remarkable coevolution between the human host andH. pylori. Perturbation of this coevolution results in dysregulation of the host-pathogen interaction, leading to oncogenic effects. This review discusses the relationship ofH. pyloriwith the human host and environment and the contribution of each of these factors to disease progression, with an emphasis on features that have been illuminated by genomic tools.

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Abd El-Ghany, Wafaa A. "Helicobacter pullorum: A potential hurdle emerging pathogen for public health." Journal of Infection in Developing Countries 14, no. 11 (November 30, 2020): 1225–30. http://dx.doi.org/10.3855/jidc.12843.

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Emerging zoonotic pathogens gain more attention due to the adverse effects on human and animal’s health and productivity. One of these zoonotic pathogens is Helicobacter pullorum (H. pullorum) which was firstly diagnosed in 1994. This bacterium is enterpathogenic in poultry and contaminates the carcasses meat during processing or improper handling. Human can get H. pullorum infection mainly through mishandling of contaminated carcasses or consumption of undercooked meat. Infection of H. pullorum in human is associated with gastroenteritis and hepatitis. Diagnosis of H. pullorum is very difficult as misdiagnosis with other enteric zoonotic pathogens like Campylobacter and other Helicobacter species is common. Unlike other types of Helicobacter, there are little information and few researches regarding prevalence, pathogenesis, diagnosis and control of H. pullorum infection either animals or human. Accordingly, this review article was prepared to give more details about H. pullorum sources of infection, pathogenicity, incidence in poultry and human as well as its treatment.

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Loman, N. J., L. A. S. Snyder, J. D. Linton, R. Langdon, A. J. Lawson, G. M. Weinstock, B. W. Wren, and M. J. Pallen. "Genome Sequence of the Emerging Pathogen Helicobacter canadensis." Journal of Bacteriology 191, no. 17 (June 19, 2009): 5566–67. http://dx.doi.org/10.1128/jb.00729-09.

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ABSTRACT We determined the genome sequence of the type strain of Helicobacter canadensis, an emerging human pathogen with diverse animal reservoirs. Potential virulence determinants carried by the genome include systems for N-linked glycosylation and capsular export. A protein-based phylogenetic analysis places H. canadensis close to Wolinella succinogenes.

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Prashar, Akriti, Mariana I. Capurro, and Nicola L. Jones. "Under the Radar: Strategies Used by Helicobacter pylori to Evade Host Responses." Annual Review of Physiology 84, no. 1 (February 10, 2022): 485–506. http://dx.doi.org/10.1146/annurev-physiol-061121-035930.

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The body depends on its physical barriers and innate and adaptive immune responses to defend against the constant assault of potentially harmful microbes. In turn, successful pathogens have evolved unique mechanisms to adapt to the host environment and manipulate host defenses. Helicobacter pylori ( Hp), a human gastric pathogen that is acquired in childhood and persists throughout life, is an example of a bacterium that is very successful at remodeling the host-pathogen interface to promote a long-term persistent infection. Using a combination of secreted virulence factors, immune subversion, and manipulation of cellular mechanisms, Hp can colonize and persist in the hostile environment of the human stomach. Here, we review the most recent and relevant information regarding how this successful pathogen overcomes gastric epithelial host defense responses to facilitate its own survival and establish a chronic infection.

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Krebes, Juliane, Richard D. Morgan, Boyke Bunk, Cathrin Spröer, Khai Luong, Raphael Parusel, Brian P. Anton, et al. "The complex methylome of the human gastric pathogen Helicobacter pylori." Nucleic Acids Research 42, no. 4 (December 2, 2013): 2415–32. http://dx.doi.org/10.1093/nar/gkt1201.

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Abstract The genome of Helicobacter pylori is remarkable for its large number of restriction-modification (R-M) systems, and strain-specific diversity in R-M systems has been suggested to limit natural transformation, the major driving force of genetic diversification in H. pylori. We have determined the comprehensive methylomes of two H. pylori strains at single base resolution, using Single Molecule Real-Time (SMRT®) sequencing. For strains 26695 and J99-R3, 17 and 22 methylated sequence motifs were identified, respectively. For most motifs, almost all sites occurring in the genome were detected as methylated. Twelve novel methylation patterns corresponding to nine recognition sequences were detected (26695, 3; J99-R3, 6). Functional inactivation, correction of frameshifts as well as cloning and expression of candidate methyltransferases (MTases) permitted not only the functional characterization of multiple, yet undescribed, MTases, but also revealed novel features of both Type I and Type II R-M systems, including frameshift-mediated changes of sequence specificity and the interaction of one MTase with two alternative specificity subunits resulting in different methylation patterns. The methylomes of these well-characterized H. pylori strains will provide a valuable resource for future studies investigating the role of H. pylori R-M systems in limiting transformation as well as in gene regulation and host interaction.

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Sharma, Cynthia M., Steve Hoffmann, Fabien Darfeuille, Jérémy Reignier, Sven Findeiß, Alexandra Sittka, Sandrine Chabas, et al. "The primary transcriptome of the major human pathogen Helicobacter pylori." Nature 464, no. 7286 (February 17, 2010): 250–55. http://dx.doi.org/10.1038/nature08756.

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Zanotti, Giuseppe, Francesca Vallese, and Nigam M. Mishra. "Function from structure: Lpp20 from the human pathogen Helicobacter pylori." Acta Crystallographica Section A Foundations and Advances 73, a2 (December 1, 2017): C240. http://dx.doi.org/10.1107/s2053273317093330.

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Pflock, Michael, Simone Kennard, Nadja Finsterer, and Dagmar Beier. "Acid-responsive gene regulation in the human pathogen Helicobacter pylori." Journal of Biotechnology 126, no. 1 (October 2006): 52–60. http://dx.doi.org/10.1016/j.jbiotec.2006.03.045.

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de Matos, A. P. Alves, F. F. Vale, and J. M. B. Vitor. "Helicobacter pylori Association with Amoeba: A Natural Reservoir of the Bacteria?" Microscopy and Microanalysis 18, S5 (August 2012): 27–28. http://dx.doi.org/10.1017/s1431927612012792.

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Helicobacter pylori is a human pathogen involved in gastritis and gastric cancer whose mode of transmission remains unknown. Association of H. pylori with humans is thought to date from remote antiquity and the bacterium has apparently evolved together with the human host. A few studies have shown the presence of H. pylori in aquatic environments, which might provide a route of transmission of the bacteria to humans. A recent study has also disclosed the association of the bacteria with Acantamoeba castellanii. Amoeba are known to harbor and promote the persistence of several human pathogens in the environment, representing a significant source of contamination in community and hospital acquired infections.

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Pulić, Ivana, Laura Cendron, Marco Salamina, Patrizia Polverino de Laureto, Dubravka Matković-Čalogović, and Giuseppe Zanotti. "Crystal structure of truncated FlgD from the human pathogen Helicobacter pylori." Journal of Structural Biology 194, no. 2 (May 2016): 147–55. http://dx.doi.org/10.1016/j.jsb.2016.02.003.

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Štefanić, Zoran, Goran Mikleušević, Marija Luić, Agnieszka Bzowska, and Ivana Leščić Ašler. "Structural characterization of purine nucleoside phosphorylase from human pathogen Helicobacter pylori." International Journal of Biological Macromolecules 101 (August 2017): 518–26. http://dx.doi.org/10.1016/j.ijbiomac.2017.03.101.

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14

Simor, Andrew E., and James L. Brunton. "Bacteremia due toHelicobacter cinaediin Two Patients with Human Immunodeficinecy Virus Infection." Canadian Journal of Infectious Diseases 3, no. 3 (1992): 139–41. http://dx.doi.org/10.1155/1992/125396.

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Helicobacter cinaedi(formerlyCampylobacter cinaedi) has been associated with enteric disease in homosexual men. The authors report two cases ofH cinaedibacteremia occurring in patients with human immunodeficiency virus (HIV) infection. These cases illustrate thatH cinaedimay act as an opportunistic pathogen in patients with HN infection or the acquired immune deficiency syndrome.

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Waldenström, Jonas, Stephen L. W. On, Richard Ottvall, Dennis Hasselquist, Clare S. Harrington, and Björn Olsen. "Avian Reservoirs and Zoonotic Potential of the Emerging Human Pathogen Helicobacter canadensis." Applied and Environmental Microbiology 69, no. 12 (December 2003): 7523–26. http://dx.doi.org/10.1128/aem.69.12.7523-7526.2003.

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ABSTRACT A polyphasic identification approach was used to investigate the taxonomic position of Campylobacter-like isolates recovered from barnacle geese (Branta leucopsis) and Canada geese (Branta candensis). Seven strains were selected from a collection of 21 isolates and analyzed by extensive phenotypic testing; four strains were characterized by 16S rRNA gene sequence analysis. The results clearly identified the bird isolates as Helicobacter canadensis, recently described as an emerging human pathogen. This is the first report of an animal reservoir for this organism and of its presence in Europe and confirms the zoonotic potential of H. canadensis.

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de Klerk, Nele, Lisa Maudsdotter, Hanna Gebreegziabher, Sunil D. Saroj, Beatrice Eriksson, Olaspers Sara Eriksson, Stefan Roos, Sara Lindén, Hong Sjölinder, and Ann-Beth Jonsson. "Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression." Infection and Immunity 84, no. 5 (February 29, 2016): 1526–35. http://dx.doi.org/10.1128/iai.00163-16.

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The human gastrointestinal tract, including the harsh environment of the stomach, harbors a large variety of bacteria, of whichLactobacillusspecies are prominent members. The molecular mechanisms by which species of lactobacilli interfere with pathogen colonization are not fully characterized. In this study, we aimed to study the effect of lactobacillus strains upon the initial attachment ofHelicobacter pylorito host cells. Here we report a novel mechanism by which lactobacilli inhibit adherence of the gastric pathogenH. pylori. In a screen withLactobacillusisolates, we found that only a few could reduce adherence ofH. pylorito gastric epithelial cells. Decreased attachment was not due to competition for space or to lactobacillus-mediated killing of the pathogen. Instead, we show that lactobacilli act onH. pyloridirectly by an effector molecule that is released into the medium. This effector molecule acts onH. pyloriby inhibiting expression of the adhesin-encoding genesabA. Finally, we verified that inhibitory lactobacilli reducedH. pyloricolonization in anin vivomodel. In conclusion, certainLactobacillusstrains affect pathogen adherence by inhibitingsabAexpression and thereby reducingH. pyloribinding capacity.

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Elbir, Haitham, Faisal Almathen, and Naser A. Alhumam. "A glimpse of the bacteriome of Hyalomma dromedarii ticks infesting camels reveals human Helicobacter pylori pathogen." Journal of Infection in Developing Countries 13, no. 11 (November 30, 2019): 1001–12. http://dx.doi.org/10.3855/jidc.11604.

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Introduction: The tick Hyalomma dromedarii is predominant in camels of Saudi Arabia and harbor multiple pathogens causing disease in humans and animals. Knowing the bacterial community of ticks is crucial for surveillance of known and newly emerging pathogens. Yet, the bacteriome of H. dromedarii remain unexplored to date. Methodology: In a cross-sectional survey, we used V3-V4 region of 16S rRNA to characterize the bacteriome of 62 whole H. dromedarii tick samples collected from camels found in Hofuf city in Saudi Arabia. Results: Sequencing results yielded 217 species incorporated into 114 genera, which in turn belong to the dominant phylum Proteobacteria (98%) followed by Firmicutes (1.38%), Actinobacteria (0.36%), Bacteroidetes (0.17%), meanwhile the phyla Cyanobacteria, Verrucomicrobia and unclassified bacteria were rarely detected. Francisella endosymbiont dominated the bacteriome of H. dromedarii ticks with average abundance of 94.37% and together with Salincoccus sp. accounted for 94.51% of the average sequences. The remaining bacteriome consisted of low abundance of potential pathogens and environmental bacteria. Of these pathogens, we found Helicobacter pylori in the tick H. dromedarii for the first time. Notably, Anaplasma, Ehrlichia and Rickettsia pathogens known to be found in H. dromedarii ticks were not detected. Conclusion: This first preliminary study advances our knowledge about the bacterial community of H. dromedarii ticks and provides a basis for pathogen surveillance and studying the influences of symbionts on vector competence. Presence of pathogens in ticks, raise concerns about potential transmission of these agents to humans or animals.

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Nishida, Kazuhiro, Takamasa Iwasawa, Atsushi Tamura, and Alan T. Lefor. "Infected Abdominal Aortic Aneurysm withHelicobacter cinaedi." Case Reports in Surgery 2016 (2016): 1–2. http://dx.doi.org/10.1155/2016/1396568.

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Helicobacter cinaediis a rare human pathogen which has various clinical manifestations such as cellulitis, bacteremia, arthritis, meningitis, and infectious endocarditis. We report an abdominal aortic aneurysm infected withHelicobacter cinaedi, treated successfully with surgical repair and long-term antimicrobial therapy.

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Waidner, Barbara, Mara Specht, Felix Dempwolff, Katharina Haeberer, Sarah Schaetzle, Volker Speth, Manfred Kist, and Peter L. Graumann. "A Novel System of Cytoskeletal Elements in the Human Pathogen Helicobacter pylori." PLoS Pathogens 5, no. 11 (November 20, 2009): e1000669. http://dx.doi.org/10.1371/journal.ppat.1000669.

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Liang, Jungang, Richard Ducatelle, Frank Pasmans, Annemieke Smet, Freddy Haesebrouck, and Bram Flahou. "Multilocus Sequence Typing of the Porcine and Human Gastric Pathogen Helicobacter suis." Journal of Clinical Microbiology 51, no. 3 (January 9, 2013): 920–26. http://dx.doi.org/10.1128/jcm.02399-12.

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Doig, P., J. W. Austin, M. Kostrzynska, and T. J. Trust. "Production of a conserved adhesin by the human gastroduodenal pathogen Helicobacter pylori." Journal of Bacteriology 174, no. 8 (1992): 2539–47. http://dx.doi.org/10.1128/jb.174.8.2539-2547.1992.

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Semrau, Antje, Susanne Gerold, Julia-Stefanie Frick, and Franz Iglauer. "Non-invasive detection and successful treatment of a Helicobacter pylori infection in a captive rhesus macaque." Laboratory Animals 51, no. 2 (September 24, 2016): 208–11. http://dx.doi.org/10.1177/0023677216669179.

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Gastritis is a commonly diagnosed condition in non-human primates used in biomedical research. As in humans, Helicobacter pylori infection may cause gastritis. The following report presents a method of non-invasive detection and a successful treatment protocol for this common pathogen.

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Simmons, Kaneatra, Clarissa Curioso, Tarsha Eason, Shannon Griffin, G. Fout, Timothy Wade, Andrey Egorov, and Swinburne Augustine. "A novel multiplexed immunoassay using salivary antibodies to detect human exposure to waterborne pathogens in drinking and recreational water (65.19)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 65.19. http://dx.doi.org/10.4049/jimmunol.186.supp.65.19.

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Abstract Water is our most important resource and the world’s supply is becoming alarmingly limited with rising concern about the high levels of microbial contamination. We are developing a novel strategy to assess human exposure to microbial contaminants in drinking and recreational water using a multiplexed, high-throughput immunoassay applying the Luminex xMAP platform. In this assay, antigens from waterborne pathogens are coupled to spectrally unique microspheres that are exposed to either pathogen-specific antibodies or human saliva. Our results indicate that multiplexed microsphere sets coated with antigens to Helicobacter pylori, Salmonella typhimurium, Escherichia coli O157:H7, Campylobacter jejuni, Toxoplasma gondii, Cryptosporidium parvum, and Giardia lamblia are able to capture both pathogen-specific antibodies and human salivary antibodies at the lowest-limit of detection of the assay. Additionally, we implemented a Design of Experiment (DoE) approach to evaluate the impact of antigen and antibody concentration on the detection level of H. pylori. From this work, we were able to generate a mathematical model describing the detection level as a function of critical process parameters to determine optimal conditions for protein coupling to Luminex beads. This immunoassay will allow for a sensitive, rapid, and cost-effective analysis of human exposure to waterborne pathogens with the potential to reduce the cost of epidemiological surveillance of waterborne infections.

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Paradowski, Leszek. "Helicobacter pylori – a still ongoing problem." Medycyna Faktów 13, no. 4 (December 31, 2020): 491–95. http://dx.doi.org/10.24292/01.mf.0420.17.

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The diagnosis and treatment of Helicobacter pylori infection are up-to-date, which is due to the frequency of human infections and the consequences of the chronic once, in most cases Helicobacter pylori infection is asymptomatic. If there are symptoms, the most common are dyspeptic complaints. In some patients Helicobacter pylori causes severe disease, mainly in stomach. This pathogen has been recognized as the main cause of the peptic ulcer, gastric cancer and MALT lymphoma. It is also known to play an important role in some other disease such essential thrombocytopenia, some types of deficiency anemia. This article discusses the current on the epidemiology of Helicobacter pylori infection, its consequences, diagnosis, treatment and the prevention of infection, information on changes in flora of digestive tract that can occur during the eradication of this bacterium, is also presented.

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Merrell, D. Scott, Maria L. Goodrich, Glen Otto, Lucy S. Tompkins, and Stanley Falkow. "pH-Regulated Gene Expression of the Gastric Pathogen Helicobacter pylori." Infection and Immunity 71, no. 6 (June 2003): 3529–39. http://dx.doi.org/10.1128/iai.71.6.3529-3539.2003.

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ABSTRACT Colonization by the gastric pathogen Helicobacter pylori has been shown to be intricately linked to the development of gastritis, ulcers, and gastric malignancy. Little is known about mechanisms employed by the bacterium that help it adapt to the hostile environment of the human stomach. In an effort to extend our knowledge of these mechanisms, we utilized spotted-DNA microarrays to characterize the response of H. pylori to low pH. Expression of approximately 7% of the bacterial genome was reproducibly altered by shift to low pH. Analysis of the differentially expressed genes led to the discovery that acid exposure leads to profound changes in motility of H. pylori, as a larger percentage of acid-exposed bacterial cells displayed motility and moved at significantly higher speeds. In contrast to previous publications, we found that expression of the bacterial virulence gene cagA was strongly repressed by acid exposure. Furthermore, this transcriptional repression was reflected at the level of protein accumulation in the H. pylori cell.

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Sukati, Suriyan, Imran Sama-ae, Gerd Katzenmeier, and Sueptrakool Wisessombat. "Evaluation of Susceptibility of the Human Pathogen Helicobacter pylori to the Antibiotic Capreomycin." Scientific World Journal 2022 (July 31, 2022): 1–12. http://dx.doi.org/10.1155/2022/8924023.

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Helicobacter pylori infection causes gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue lymphoma, and gastric cancer and can also promote thrombosis. It is estimated that approximately 4.5 billion individuals are infected, thus rendering H. pylori the most prevalent microbial pathogen. Currently established regimes for antibiotic treatment are massively challenged by increasing drug resistance and the development of novel antimicrobial therapies is urgently required. The antibiotic capreomycin is clinically used against multiple drug-resistant strains of Mycobacterium tuberculosis. It targets the complex between TlyA, a hemolysin- and RNA-binding protein, and the bacterial rRNA. In this study we have explored the possible antibacterial effects of capreomycin against several strains of H. pylori and found only moderate activity which was comparable to metronidazole-resistant strains. Molecular docking of capreomycin to TlyA proteins from H. pylori and M. tuberculosis identified several residues within TlyA which interact with the drug; however, binding affinities of H. pylori– TlyA for capreomycin appear to be higher than those of Mycobacterium– TlyA. The data suggest that capreomycin may warrant further investigations into its potential use as antibiotic against H. pylori.

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Salama, Nina R., Mara L. Hartung, and Anne Müller. "Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori." Nature Reviews Microbiology 11, no. 6 (May 8, 2013): 385–99. http://dx.doi.org/10.1038/nrmicro3016.

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Quarantini, Sandra, Laura Cendron, and Giuseppe Zanotti. "Crystal structure of the secreted protein HP1454 from the human pathogen Helicobacter pylori." Proteins: Structure, Function, and Bioinformatics 82, no. 10 (June 9, 2014): 2868–73. http://dx.doi.org/10.1002/prot.24608.

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Maier, R. J. "Use of molecular hydrogen as an energy substrate by human pathogenic bacteria." Biochemical Society Transactions 33, no. 1 (February 1, 2005): 83–85. http://dx.doi.org/10.1042/bst0330083.

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Molecular hydrogen is produced as a fermentation by-product in the large intestine of animals and its production can be correlated with the digestibility of the carbohydrates consumed. Pathogenic Helicobacter species (Helicobacter pylori and H. hepaticus) have the ability to use H2 through a respiratory hydrogenase, and it was demonstrated that the gas is present in the tissues colonized by these pathogens (the stomach and the liver respectively of live animals). Mutant strains of H. pylori unable to use H2 are deficient in colonizing mice compared with the parent strain. On the basis of available annotated gene sequence information, the enteric pathogen Salmonella, like other enteric bacteria, contains three putative membrane-associated H2-using hydrogenase enzymes. From the analysis of gene-targeted mutants it is concluded that each of the three membrane-bound hydrogenases of Salmonella enterica serovar Typhimurium are coupled with an H2-oxidizing respiratory pathway. From microelectrode probe measurements on live mice, H2 could be detected at approx. 50 μM levels within the tissues (liver and spleen), which are colonized by Salmonella. The half-saturation affinity of whole cells of these pathogens for H2 is much less than this, so it is expected that the (H2-utilizing) hydrogenase enzymes be saturated with the reducing substrate in vivo. All three enteric NiFe hydrogenase enzymes contribute to virulence of the bacterium in a typhoid fever-mouse model, and the combined removal of all three hydrogenases resulted in a strain that is avirulent and (in contrast with the parent strain) one that is not able to pass the intestinal tract to invade liver or spleen tissue. It is proposed that H2 utilization and specifically its oxidation, coupled with a respiratory pathway, is required for energy production to permit growth and maintain efficient virulence of a number of pathogenic bacteria during infection of animals. These would be expected to include the Campylobacter jejuni, a bacterium closely related to Helicobacter, as well as many enteric bacteria (Escherichia coli, Shigella and Yersinia species).

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Palrasu, Manikandan, Elena Zaika, Kodisundaram Paulrasu, Ravindran Caspa Gokulan, Giovanni Suarez, Jianwen Que, Wael El-Rifai, Richard M. Peek, Monica Garcia-Buitrago, and Alexander I. Zaika. "Helicobacter pylori pathogen inhibits cellular responses to oncogenic stress and apoptosis." PLOS Pathogens 18, no. 6 (June 29, 2022): e1010628. http://dx.doi.org/10.1371/journal.ppat.1010628.

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Helicobacter pylori (H. pylori) is a common gastric pathogen that infects approximately half of the world’s population. Infection with H. pylori can lead to diverse pathological conditions, including chronic gastritis, peptic ulcer disease, and cancer. The latter is the most severe consequence of H. pylori infection. According to epidemiological studies, gastric infection with H. pylori is the strongest known risk factor for non-cardia gastric cancer (GC), which remains one of the leading causes of cancer-related deaths worldwide. However, it still remains to be poorly understood how host-microbe interactions result in cancer development in the human stomach. Here we focus on the H. pylori bacterial factors that affect the host ubiquitin proteasome system. We investigated E3 ubiquitin ligases SIVA1 and ULF that regulate p14ARF (p19ARF in mice) tumor suppressor. ARF plays a key role in regulation of the oncogenic stress response and is frequently inhibited during GC progression. Expression of ARF, SIVA1 and ULF proteins were investigated in gastroids, H. pylori-infected mice and human gastric tissues. The role of the H. pylori type IV secretion system was assessed using various H. pylori isogenic mutants. Our studies demonstrated that H. pylori infection results in induction of ULF, decrease in SIVA1 protein levels, and subsequent ubiquitination and degradation of p14ARF tumor suppressor. Bacterial CagA protein was found to sequentially bind to SIVA1 and ULF proteins. This process is regulated by CagA protein phosphorylation at the EPIYA motifs. Downregulation of ARF protein leads to inhibition of cellular apoptosis and oncogenic stress response that may promote gastric carcinogenesis.

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Bumann, Dirk, Sevil Aksu, Meike Wendland, Katharina Janek, Uschi Zimny-Arndt, Nicolas Sabarth, Thomas F. Meyer, and Peter R. Jungblut. "Proteome Analysis of Secreted Proteins of the Gastric Pathogen Helicobacter pylori." Infection and Immunity 70, no. 7 (July 2002): 3396–403. http://dx.doi.org/10.1128/iai.70.7.3396-3403.2002.

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ABSTRACT Secreted proteins (the secretome) of the human pathogen Helicobacter pylori may mediate important pathogen-host interactions, but such proteins are technically difficult to analyze. Here, we report on a comprehensive secretome analysis that uses protein-free culture conditions to minimize autolysis, an efficient recovery method for extracellular proteins, and two-dimensional gel electrophoresis followed by peptide mass fingerprinting for protein resolution and identification. Twenty-six of the 33 separated secreted proteins were identified. Among them were six putative oxidoreductases that may be involved in the modification of protein-disulfide bonds, three flagellar proteins, three defined fragments of the vacuolating toxin VacA, the serine protease HtrA, and eight proteins of unknown function. A cleavage site for the amino-terminal passenger domain of VacA between amino acids 991 and 992 was determined by collision-induced dissociation mass spectrometry. Several of the secreted proteins are interesting targets for antimicrobial chemotherapy and vaccine development.

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Lettl, Clara, and Wolfgang Fischer. "Export von Gefahrgut: Helicobacter pylori und sein CagA-Protein." BIOspektrum 26, no. 6 (October 14, 2020): 597–99. http://dx.doi.org/10.1007/s12268-020-1454-7.

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Abstract Pathogenic bacteria often utilize type IV secretion systems to interact with host cells and to modify their microenvironment in a favourable way. The human pathogen Helicobacter pylori produces such a system to inject only a single protein, CagA, into gastric cells, but this injection represents a major risk factor for gastric cancer development. Here, we discuss the unusual structure of the Cag secretion nanomachine and other features that make it unique among bacterial protein transporters.

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Shetty, Vignesh, Richard Lobo, Nimmy Kumar, Ramachandra Lingadakai, Ganesh C Pai, Girish Balaraju, and Mamatha Ballal. "ANTIMICROBIAL ACTIVITY OF ANISOCHILUS CARNOSUS (L.F.) WALL AGAINST THE HUMAN GASTRIC PATHOGEN HELICOBACTER PYLORI." Asian Journal of Pharmaceutical and Clinical Research 10, no. 10 (September 1, 2017): 292. http://dx.doi.org/10.22159/ajpcr.2017.v10i10.20304.

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Objective: The prevalence of Helicobacter pylori in India is high, and majority leads to severe gastrointestinal infections. Existing treatment regimens for H. pylori infections have increased failure rates and adverse side effects that desire the search for an effective substitute therapy. Anisochilus carnosus (L.f.) wall (Lamiaceae), a herb which grows once in a year at high elevation is used widely in traditional treatment for the complaints of gastric ulcer and skin diseases. The present study was performed to assess the antibacterial activity of A. carnosus (L.f.) wall, against clinical isolates of H. pylori in vitro.Methods: A. carnosus leaves were collected-dried and extracted with water and ethanol by cold maceration with ethanol by soxhlet method. The minimum inhibitory concentration (MIC) of extracts was made and tested against 32 clinical and 1 reference strains of H. pylori. Results: A. carnosus (L.f.) wall inhibited the growth of most of the clinical H. pylori strains. The MIC of A. carnosus (L.f.) wall extracted by cold maceration (aqueous and ethanol) and Soxhlet apparatus (ethanol) ranged from 500 to 62.5 μg/ml, and the majority of the clinical H. pylori strains were inhibited at the MIC of 500 μg/ml of aqueous, ethanol, and Soxhlet ethanol extraction were 63.63%, 43.75%, and 71.87%, respectively.Conclusion: A. carnosus (L.f.) wall is an efficient inhibitor of H. pylori growth in vitro. A. carnosus (L.f.) wall revealed enormous therapeutic potential to H. pylori infection as it was extremely active in the suppression of H. pylori. Hence, it can be taken as a potential agent against several H. pylori linked gastric pathogenic progressions.

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Kondadi, P. K., M. Rossi, B. Twelkmeyer, M. J. Schur, J. Li, T. Schott, L. Paulin, et al. "Identification and Characterization of a Lipopolysaccharide ,2,3-Sialyltransferase from the Human Pathogen Helicobacter bizzozeronii." Journal of Bacteriology 194, no. 10 (March 9, 2012): 2540–50. http://dx.doi.org/10.1128/jb.00126-12.

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Alm, Richard A., Lo-See L. Ling, Donald T. Moir, Benjamin L. King, Eric D. Brown, Peter C. Doig, Douglas R. Smith, et al. "Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori." Nature 397, no. 6715 (January 14, 1999): 176–80. http://dx.doi.org/10.1038/16495.

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Jalava, Katri. "A Cultured Strain of "Helicobacter heilmannii," a Human Gastric Pathogen, Identified as H. bizzozeronii: Evidence for Zoonotic Potential of Helicobacter." Emerging Infectious Diseases 7, no. 6 (December 2001): 1036–38. http://dx.doi.org/10.3201/eid0706.010622.

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Jarzab, Miroslaw, Gernot Posselt, Nicole Meisner-Kober, and Silja Wessler. "Helicobacter pylori-Derived Outer Membrane Vesicles (OMVs): Role in Bacterial Pathogenesis?" Microorganisms 8, no. 9 (August 31, 2020): 1328. http://dx.doi.org/10.3390/microorganisms8091328.

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Persistent infections with the human pathogen Helicobacter pylori (H. pylori) have been closely associated with the induction and progression of a wide range of gastric disorders, including acute and chronic gastritis, ulceration in the stomach and duodenum, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma. The pathogenesis of H. pylori is determined by a complicated network of manifold mechanisms of pathogen–host interactions, which involves a coordinated interplay of H. pylori pathogenicity and virulence factors with host cells. While these molecular and cellular mechanisms have been intensively investigated to date, the knowledge about outer membrane vesicles (OMVs) derived from H. pylori and their implication in bacterial pathogenesis is not well developed. In this review, we summarize the current knowledge on H. pylori-derived OMVs.

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Vannini, Andrea, Davide Roncarati, Federico D’Agostino, Federico Antoniciello, and Vincenzo Scarlato. "Insights into the Orchestration of Gene Transcription Regulators in Helicobacter pylori." International Journal of Molecular Sciences 23, no. 22 (November 8, 2022): 13688. http://dx.doi.org/10.3390/ijms232213688.

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Bacterial pathogens employ a general strategy to overcome host defenses by coordinating the virulence gene expression using dedicated regulatory systems that could raise intricate networks. During the last twenty years, many studies of Helicobacter pylori, a human pathogen responsible for various stomach diseases, have mainly focused on elucidating the mechanisms and functions of virulence factors. In parallel, numerous studies have focused on the molecular mechanisms that regulate gene transcription to attempt to understand the physiological changes of the bacterium during infection and adaptation to the environmental conditions it encounters. The number of regulatory proteins deduced from the genome sequence analyses responsible for the correct orchestration of gene transcription appears limited to 14 regulators and three sigma factors. Furthermore, evidence is accumulating for new and complex circuits regulating gene transcription and H. pylori virulence. Here, we focus on the molecular mechanisms used by H. pylori to control gene transcription as a function of the principal environmental changes.

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Stent, Andrew, Alison L. Every, and Philip Sutton. "Helicobacter pyloridefense against oxidative attack." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 6 (March 15, 2012): G579—G587. http://dx.doi.org/10.1152/ajpgi.00495.2011.

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Helicobacter pylori is a microaerophilic, gram-negative pathogen of the human stomach. Despite the chronic active gastritis that develops following colonization, H. pylori is able to persist unharmed in the stomach for decades. Much of the damage caused by gastric inflammation results from the accumulation of reactive oxygen/nitrogen species within the stomach environment, which can induce oxidative damage in a wide range of biological molecules. Without appropriate defenses, this oxidative damage would be able to rapidly kill nearby H. pylori, but the organism employs a range of measures, including antioxidant enzymes, biological repair systems, and inhibitors of oxidant generation, to counter the attack. Despite the variety of measures employed to defend against oxidative injury, these processes are intimately interdependent, and any deficiency within the antioxidant system is generally sufficient to cause substantial impairment of H. pylori viability and persistence. This review provides an overview of the development of oxidative stress during H. pylori gastritis and examines the methods the organism uses to survive the resultant damage.

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Devi, Singamaneni Haritha, Todd D. Taylor, Tiruvayipati Suma Avasthi, Shinji Kondo, Yutaka Suzuki, Francis Megraud, and Niyaz Ahmed. "Genome of Helicobacter pylori Strain 908." Journal of Bacteriology 192, no. 24 (October 15, 2010): 6488–89. http://dx.doi.org/10.1128/jb.01110-10.

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ABSTRACT Helicobacter pylori is a genetically diverse and coevolved pathogen inhabiting human gastric niches and leading to a spectrum of gastric diseases in susceptible populations. We describe the genome sequence of H. pylori 908, which was originally isolated from an African patient living in France who suffered with recrudescent duodenal ulcer disease. The strain was found to be phylogenetically related to H. pylori J99, and its comparative analysis revealed several specific genome features and novel insertion-deletion and substitution events. The genome sequence revealed several strain-specific deletions and/or gain of genes exclusively present in HP908 compared with different sequenced genomes already available in the public domain. Comparative and functional genomics of HP908 and its subclones will be important in understanding genomic plasticity and the capacity to colonize and persist in a changing host environment.

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Rimbara, Emiko, Masato Suzuki, Hidenori Matsui, Masahiko Nakamura, Misako Morimoto, Chihiro Sasakawa, Hiroki Masuda, et al. "Isolation and characterization of Helicobacter suis from human stomach." Proceedings of the National Academy of Sciences 118, no. 13 (March 22, 2021): e2026337118. http://dx.doi.org/10.1073/pnas.2026337118.

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Helicobacter suis, a bacterial species naturally hosted by pigs, can colonize the human stomach in the context of gastric diseases such as gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Because H. suis has been successfully isolated from pigs, but not from humans, evidence linking human H. suis infection to gastric diseases has remained incomplete. In this study, we successfully in vitro cultured H. suis directly from human stomachs. Unlike Helicobacter pylori, the viability of H. suis decreases significantly on neutral pH; therefore, we achieved this using a low-pH medium for transport of gastric biopsies. Ultimately, we isolated H. suis from three patients with gastric diseases, including gastric MALT lymphoma. Successful eradication of H. suis yielded significant improvements in endoscopic and histopathological findings. Oral infection of mice with H. suis clinical isolates elicited gastric and systemic inflammatory responses; in addition, progression of gastric mucosal metaplasia was observed 4 mo postinfection. Because H. suis could be isolated from the stomachs of infected mice, our findings satisfied Koch’s postulates. Although further prospective clinical studies are needed, H. suis, like H. pylori, is likely a gastric pathogen in humans. Furthermore, comparative genomic analysis of H. suis using complete genomes of clinical isolates revealed that the genome of each H. suis isolate contained highly plastic genomic regions encoding putative strain-specific virulence factors, including type IV secretion system–associated genes, and that H. suis isolates from humans and pigs were genetically very similar, suggesting possible pig-to-human transmission.

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Kersulyte, Dangeruta, Asish K. Mukhopadhyay, Billie Velapatiño, WanWen Su, ZhiJun Pan, Claudia Garcia, Virginia Hernandez, et al. "Differences in Genotypes of Helicobacter pylori from Different Human Populations." Journal of Bacteriology 182, no. 11 (June 1, 2000): 3210–18. http://dx.doi.org/10.1128/jb.182.11.3210-3218.2000.

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ABSTRACT DNA motifs at several informative loci in more than 500 strains ofHelicobacter pylori from five continents were studied by PCR and sequencing to gain insights into the evolution of this gastric pathogen. Five types of deletion, insertion, and substitution motifs were found at the right end of the H. pylori cagpathogenicity island. Of the three most common motifs, type I predominated in Spaniards, native Peruvians, and Guatemalan Ladinos (mixed Amerindian-European ancestry) and also in native Africans and U.S. residents; type II predominated among Japanese and Chinese; and type III predominated in Indians from Calcutta. Sequences in the cagA gene and in vacAm1 type alleles of the vacuolating cytotoxin gene (vacA) of strains from native Peruvians were also more like those from Spaniards than those from Asians. These indications of relatedness of Latin American and Spanish strains, despite the closer genetic relatedness of Amerindian and Asian people themselves, lead us to suggest that H. pylori may have been brought to the New World by European conquerors and colonists about 500 years ago. This thinking, in turn, suggests that H. pylori infection might have become widespread in people quite recently in human evolution.

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Roth, Kevin A., Sharookh B. Kapadia, Steven M. Martin, and Robin G. Lorenz. "Cellular Immune Responses Are Essential for the Development of Helicobacter felis-Associated Gastric Pathology." Journal of Immunology 163, no. 3 (August 1, 1999): 1490–97. http://dx.doi.org/10.4049/jimmunol.163.3.1490.

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Abstract The bacteria Helicobacter pylori is a major human pathogen that infects over half of the world’s population. Infection initiates a series of changes in the gastric mucosa, beginning with atrophic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and gastric adenocarcinoma. Although this cascade of events clearly occurs, little is known about the role of the host immune response in disease progression. We have utilized the C57BL/6 Helicobacter felis mouse model to critically analyze the role of the adaptive immune response in the development of Helicobacter-associated gastric pathology. Infection of B and T cell-deficient RAG-1−/− mice or T cell-deficient TCRβδ−/− mice with H. felis resulted in high levels of colonization, but no detectable gastric pathology. Conversely, infection of B cell-deficient μMT mice resulted in severe gastric alterations identical with those seen in immunocompetent C57BL/6-infected mice, including gastric mucosal hyperplasia and intestinal metaplasia. These results demonstrate that the host T cell response is a critical mediator of Helicobacter-associated gastric pathology, and that B cells and their secreted Abs are not the effectors of the immune-mediated gastric pathology seen after H. felis infection. These results indicate that in addition to specific Helicobacter virulence factors, the host immune response is an important determinant of Helicobacter-associated disease.

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Bäckhed, Fredrik, Elisabeth Torstensson, Delphine Seguin, Agneta Richter-Dahlfors, and Bachra Rokbi. "Helicobacter pylori Infection Induces Interleukin-8 Receptor Expression in the Human Gastric Epithelium." Infection and Immunity 71, no. 6 (June 2003): 3357–60. http://dx.doi.org/10.1128/iai.71.6.3357-3360.2003.

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ABSTRACT The gastric pathogen Helicobacter pylori is known to activate multiple proinflammatory signaling pathways in epithelial cells. In this study, we addressed the question of whether expression of the interleukin-8 receptors IL-8RA (CXCR1) and IL-8RB (CXCR2) is upregulated in H. pylori-infected human gastric biopsy samples. Biopsy samples from patients infected with H. pylori strains harboring the cag pathogenicity island (PAI) expressed larger amounts of both receptors. In addition, IL-8RB expression was induced in the gastric epithelial cell line AGS upon infection with a clinical isolate containing the cag PAI, while a strain lacking the cag PAI did not. Our finding suggests that gastric epithelial cells express IL-8R in response to H. pylori infection.

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Brito, D., C. Serrano, C. Peres, A. Delgado, A. Pereira, M. Oleastro, and L. Monteiro. "LACTOBACILLI FROM FERMENTED PORTUGUESE TABLE-OLIVES ARE ABLE TO INHIBIT THE HUMAN PATHOGEN HELICOBACTER PYLORI." Acta Horticulturae, no. 949 (May 2012): 463–68. http://dx.doi.org/10.17660/actahortic.2012.949.68.

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Bauer, Bianca, and Thomas F. Meyer. "The Human Gastric Pathogen Helicobacter pylori and Its Association with Gastric Cancer and Ulcer Disease." Ulcers 2011 (July 18, 2011): 1–23. http://dx.doi.org/10.1155/2011/340157.

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With the momentous discovery in the 1980's that a bacterium, Helicobacter pylori, can cause peptic ulcer disease and gastric cancer, antibiotic therapies and prophylactic measures have been successful, only in part, in reducing the global burden of these diseases. To date, ~700,000 deaths worldwide are still attributable annually to gastric cancer alone. Here, we review H. pylori's contribution to the epidemiology and histopathology of both gastric cancer and peptic ulcer disease. Furthermore, we examine the host-pathogen relationship and H. pylori biology in context of these diseases, focusing on strain differences, virulence factors (CagA and VacA), immune activation and the challenges posed by resistance to existing therapies. We consider also the important role of host-genetic variants, for example, in inflammatory response genes, in determining infection outcome and the role of H. pylori in other pathologies—some accepted, for example, MALT lymphoma, and others more controversial, for example, idiopathic thrombocytic purpura. More recently, intriguing suggestions that H. pylori has protective effects in GERD and autoimmune diseases, such as asthma, have gained momentum. Therefore, we consider the basis for these suggestions and discuss the potential impact for future therapeutic rationales.

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Alm, Richard A., Lo-See L. Ling, Donald T. Moir, Benjamin L. King, Eric D. Brown, Peter C. Doig, Douglas R. Smith, et al. "Erratum: Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori." Nature 397, no. 6721 (February 1999): 719. http://dx.doi.org/10.1038/17837.

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Ahmed, Niyaz, Ahmed A. Majeed, Irshad Ahmed, M. Abid Hussain, Ayesha Alvi, S. Manjulata Devi, Mohammed Rizwan, Akash Ranjan, Leonardo A. Sechi, and Francis Mégraud. "genoBASE pylori: A genotype search tool and database of the human gastric pathogen Helicobacter pylori." Infection, Genetics and Evolution 7, no. 4 (July 2007): 463–68. http://dx.doi.org/10.1016/j.meegid.2007.01.006.

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Dailidiene, Daiva, Giedrius Dailide, Keiji Ogura, Maojun Zhang, Asish K. Mukhopadhyay, Kathryn A. Eaton, Giovanni Cattoli, Johannes G. Kusters, and Douglas E. Berg. "Helicobacter acinonychis: Genetic and Rodent Infection Studies of a Helicobacter pylori-Like Gastric Pathogen of Cheetahs and Other Big Cats." Journal of Bacteriology 186, no. 2 (January 15, 2004): 356–65. http://dx.doi.org/10.1128/jb.186.2.356-365.2004.

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ABSTRACT Insights into bacterium-host interactions and genome evolution can emerge from comparisons among related species. Here we studied Helicobacter acinonychis (formerly H. acinonyx), a species closely related to the human gastric pathogen Helicobacter pylori. Two groups of strains were identified by randomly amplified polymorphic DNA fingerprinting and gene sequencing: one group from six cheetahs in a U.S. zoo and two lions in a European circus, and the other group from a tiger and a lion-tiger hybrid in the same circus. PCR and DNA sequencing showed that each strain lacked the cag pathogenicity island and contained a degenerate vacuolating cytotoxin (vacA) gene. Analyses of nine other genes (glmM, recA, hp519, glr, cysS, ppa, flaB, flaA, and atpA) revealed a ∼2% base substitution difference, on average, between the two H. acinonychis groups and a ∼8% difference between these genes and their homologs in H. pylori reference strains such as 26695. H. acinonychis derivatives that could chronically infect mice were selected and were found to be capable of persistent mixed infection with certain H. pylori strains. Several variants, due variously to recombination or new mutation, were found after 2 months of mixed infection. H. acinonychis ' modest genetic distance from H. pylori, its ability to infect mice, and its ability to coexist and recombine with certain H. pylori strains in vivo should be useful in studies of Helicobacter infection and virulence mechanisms and studies of genome evolution.

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Bansil, Rama, Maira A. Constantino, Clover Su-Arcaro, Wentian Liao, Zeli Shen, and James G. Fox. "Motility of Different Gastric Helicobacter spp." Microorganisms 11, no. 3 (March 1, 2023): 634. http://dx.doi.org/10.3390/microorganisms11030634.

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Helicobacter spp., including the well-known human gastric pathogen H. pylori, can cause gastric diseases in humans and other mammals. They are Gram-negative bacteria that colonize the gastric epithelium and use their multiple flagella to move across the protective gastric mucus layer. The flagella of different Helicobacter spp. vary in their location and number. This review focuses on the swimming characteristics of different species with different flagellar architectures and cell shapes. All Helicobacter spp. use a run-reverse-reorient mechanism to swim in aqueous solutions, as well as in gastric mucin. Comparisons of different strains and mutants of H. pylori varying in cell shape and the number of flagella show that their swimming speed increases with an increasing number of flagella and is somewhat enhanced with a helical cell body shape. The swimming mechanism of H. suis, which has bipolar flagella, is more complex than that of unipolar H. pylori. H. suis exhibits multiple modes of flagellar orientation while swimming. The pH-dependent viscosity and gelation of gastric mucin significantly impact the motility of Helicobacter spp. In the absence of urea, these bacteria do not swim in mucin gel at pH < 4, even though their flagellar bundle rotates.

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Journal articles on the topic 'Human Pathogen Helicobacter'

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