Displaying publications 41 - 60 of 222 in total

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  1. Kaur G, Naing NN
    Malays J Med Sci, 2003 Jul;10(2):66-70.
    PMID: 23386799 MyJurnal
    The objective of this study was to determine the prevalence and ethnic distribution of Helicobacter pylori infection in an endoscoped population in North Eastern Peninsular Malaysia.
    Matched MeSH terms: Helicobacter pylori
  2. Goh KL, Chan WK, Shiota S, Yamaoka Y
    Helicobacter, 2011 Sep;16 Suppl 1:1-9.
    PMID: 21896079 DOI: 10.1111/j.1523-5378.2011.00874.x
    This review summarizes studies on the epidemiology and public health implications of Helicobacter pylori published in peer-reviewed journals from April 2010 through March 2011. Prevalence rates vary widely between different geographical regions and ethnic groups. An interesting study from the USA identified the degree of African ancestry as an independent predictor of H. pylori infection. Two studies have demonstrated early childhood as the period of transmission of infection and identified an infected sibling as an important risk factor. An oral-oral route of spread has been substantiated with several studies showing the presence of H. pylori in the oral cavity. Studies have shown the presence of H. pylori in drinking water and the role of poor living conditions and sanitation in H. pylori infection, supporting an oral-fecal route of spread. Screening for H. pylori as a gastric cancer pre-screening strategy has been described in Japan, and the importance of H. pylori eradication as a gastric cancer-prevention strategy has now been further emphasized in Japanese guidelines. Two studies have shown a decrease in the burden of dyspepsia and peptic ulcer disease with H. pylori eradication.
    Matched MeSH terms: Helicobacter pylori/isolation & purification; Helicobacter pylori/physiology
  3. Ahmad N, Zakaria WR, Mohamed R
    Helicobacter, 2011 Feb;16(1):47-51.
    PMID: 21241412 DOI: 10.1111/j.1523-5378.2010.00816.x
    The prevalence of antibiotic resistance varies in geographic areas. The information on the antibiotic susceptibility patterns of Helicobacter pylori (H. pylori) in our local setting is therefore relevant as a guide for the treatment options.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/isolation & purification
  4. Chua EG, Wise MJ, Khosravi Y, Seow SW, Amoyo AA, Pettersson S, et al.
    DNA Res, 2017 Feb 01;24(1):37-49.
    PMID: 27803027 DOI: 10.1093/dnares/dsw046
    Helicobacter pylori is a highly successful gastric pathogen. High genomic plasticity allows its adaptation to changing host environments. Complete genomes of H. pylori clinical isolate UM032 and its mice-adapted serial derivatives 298 and 299, generated using both PacBio RS and Illumina MiSeq sequencing technologies, were compared to identify novel elements responsible for host-adaptation. The acquisition of a jhp0562-like allele, which encodes for a galactosyltransferase, was identified in the mice-adapted strains. Our analysis implies a new β-1,4-galactosyltransferase role for this enzyme, essential for Ley antigen expression. Intragenomic recombination between babA and babB genes was also observed. Further, we expanded on the list of candidate genes whose expression patterns have been mediated by upstream homopolymer-length alterations to facilitate host adaption. Importantly, greater than four-fold reduction of mRNA levels was demonstrated in five genes. Among the down-regulated genes, three encode for outer membrane proteins, including BabA, BabB and HopD. As expected, a substantial reduction in BabA protein abundance was detected in mice-adapted strains 298 and 299 via Western analysis. Our results suggest that the expression of Ley antigen and reduced outer membrane protein expressions may facilitate H. pylori colonisation of mouse gastric epithelium.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/physiology
  5. Ansari S, Yamaoka Y
    Expert Rev Anti Infect Ther, 2020 10;18(10):987-996.
    PMID: 32536287 DOI: 10.1080/14787210.2020.1782739
    Introduction Helicobacter pylori causes, via the influence of several virulence factors, persistent infection of the stomach, which leads to severe complications. Vacuolating cytotoxin A (VacA) is observed in almost all clinical strains of H. pylori; however, only some strains produce the toxigenic and pathogenic VacA, which is influenced by the gene sequence variations. VacA exerts its action by causing cell vacuolation and apoptosis. We performed a PubMed search to review the latest literatures published in English language. Areas covered Articles regarding H. pylori VacA and its genotypes, architecture, internalization, and role in gastric infection and pathogenicity are reviewed. We included the search for recently published literature until January 2020. Expert opinion H. pylori VacA plays a crucial role in severe gastric pathogenicity. In addition, VacA mediated in vivo bacterial survival leads to persistent infection and an enhanced bacterial evasion from the action of antibiotics and the innate host defense system, which leads to drug evasion. VacA as a co-stimulator for the CagA phosphorylation may exert a synergistic effect playing an important role in the CagA-mediated pathogenicity.
    Matched MeSH terms: Helicobacter pylori/genetics; Helicobacter pylori/pathogenicity*
  6. Amjad N, Osman HA, Razak NA, Kassian J, Din J, bin Abdullah N
    World J Gastroenterol, 2010 Sep 21;16(35):4443-7.
    PMID: 20845512
    AIM: To study the presence of Helicobacter pylori (H. pylori) virulence factors and clinical outcome in H. pylori infected patients.

    METHODS: A prospective analysis of ninety nine H. pylori-positive patients who underwent endoscopy in our Endoscopy suite were included in this study. DNA was isolated from antral biopsy samples and the presence of cagA, iceA, and iceA2 genotypes were determined by polymerase chain reaction and a reverse hybridization technique. Screening for H. pylori infection was performed in all patients using the rapid urease test (CLO-Test).

    RESULTS: From a total of 326 patients who underwent endoscopy for upper gastrointestinal symptoms, 99 patients were determined to be H. pylori-positive. Peptic ulceration was seen in 33 patients (33%). The main virulence strain observed in this cohort was the cagA gene isolated in 43 patients. cagA was associated with peptic ulcer pathology in 39.5% (17/43) and in 28% (16/56) of non-ulcer patients. IceA1 was present in 29 patients (29%) and iceA2 in 15 patients (15%). Ulcer pathology was seen in 39% (11/29) of patients with iceA1, while 31% (22/70) had normal findings. The corresponding values for iceA2 were 33% (5/15) and 33% (28/84), respectively.

    CONCLUSION: Virulence factors were not common in our cohort. The incidence of factors cagA, iceA1 and iceA2 were very low although variations were noted in different ethnic groups.

    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/pathogenicity
  7. Wong EHJ, Ng CG, Goh KL, Vadivelu J, Ho B, Loke MF
    Sci Rep, 2018 01 23;8(1):1409.
    PMID: 29362474 DOI: 10.1038/s41598-018-19697-0
    The biofilm-forming-capability of Helicobacter pylori has been suggested to be among factors influencing treatment outcome. However, H. pylori exhibit strain-to-strain differences in biofilm-forming-capability. Metabolomics enables the inference of spatial and temporal changes of metabolic activities during biofilm formation. Our study seeks to examine the differences in metabolome of low and high biofilm-formers using the metabolomic approach. Eight H. pylori clinical strains with different biofilm-forming-capability were chosen for metabolomic analysis. Bacterial metabolites were extracted using Bligh and Dyer method and analyzed by Liquid Chromatography/Quadrupole Time-of-Flight mass spectrometry. The data was processed and analyzed using the MassHunter Qualitative Analysis and the Mass Profiler Professional programs. Based on global metabolomic profiles, low and high biofilm-formers presented as two distinctly different groups. Interestingly, low-biofilm-formers produced more metabolites than high-biofilm-formers. Further analysis was performed to identify metabolites that differed significantly (p-value pylori is complex and probably driven by the bacterium' endogenous metabolism. Understanding the underlying metabolic differences between low and high biofilm-formers may enhance our current understanding of pathogenesis, extragastric survival and transmission of H. pylori infections.
    Matched MeSH terms: Helicobacter pylori/metabolism; Helicobacter pylori/physiology*
  8. Ansari S, Yamaoka Y
    Toxins (Basel), 2019 Nov 19;11(11).
    PMID: 31752394 DOI: 10.3390/toxins11110677
    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.
    Matched MeSH terms: Helicobacter pylori/growth & development; Helicobacter pylori/pathogenicity*
  9. Loke MF, Ng CG, Vilashni Y, Lim J, Ho B
    Sci Rep, 2016 05 25;6:26784.
    PMID: 27222005 DOI: 10.1038/srep26784
    Helicobacter pylori may reside in the human stomach as two morphological forms: the culturable spiral form and the viable but non-culturable (VBNC) coccoid form. This bacterium transforms from spiral to coccoid under in vitro suboptimal conditions. However, both spiral and coccoid have demonstrated its infectivity in laboratory animals, suggesting that coccoid may potentially be involved in the transmission of H. pylori. To determine the relevance of the coccoid form in viability and infectivity, we compared the protein profiles of H. pylori coccoids obtained from prolonged (3-month-old) culture with that of 3-day-old spirals of two H. pylori standard strains using SWATH (Sequential Window Acquisition of all Theoretical mass spectra)-based approach. The protein profiles reveal that the coccoids retained basal level of metabolic proteins and also high level of proteins that participate in DNA replication, cell division and biosynthesis demonstrating that coccoids are viable. Most interestingly, these data also indicate that the H. pylori coccoids possess higher level of proteins that are involved in virulence and carcinogenesis than their spiral counterparts. Taken together, these findings have important implications in the understanding on the pathogenesis of H. pylori-induced gastroduodenal diseases, as well as the probable transmission mode of this bacterium.
    Matched MeSH terms: Helicobacter pylori/drug effects; Helicobacter pylori/genetics; Helicobacter pylori/physiology*; Helicobacter pylori/ultrastructure
  10. Goh KL, Cheah PL, Navaratnam P, Chin SC, Xiao SD
    J Dig Dis, 2007 Aug;8(3):139-42.
    PMID: 17650225
    The gastric biopsy urease test is an accurate and robust diagnostic test for Helicobacter pylori infection. Large endoscopy units use their own homemade unbuffered ultra-rapid urease test for diagnosis of H. pylori infection but several commercial rapid urease tests are available.
    Matched MeSH terms: Helicobacter pylori/enzymology; Helicobacter pylori/metabolism
  11. Vilaichone RK, Quach DT, Yamaoka Y, Sugano K, Mahachai V
    Asian Pac J Cancer Prev, 2018 May 26;19(5):1411-1413.
    PMID: 29802708
    Objective: Antibiotic resistance has significantly impact on eradication rates for H. pylori infection and remains
    important cause of treatment failure worldwide including ASEAN countries. The aim of this study was to survey
    the prevalence and antibiotic resistant pattern of H. pylori infection in ASEAN. Methods: This study was a survey among
    26 experts from 9 ASEAN countries including Thailand, Cambodia, Indonesia, Laos, Malaysia, Myanmar, Philippines,
    Singapore and Vietnam whom attended a meeting to develop the ASEAN consensus on H. pylori management in Bangkok
    in November 2015. A questionnaire was sent to each member of the consensus meeting. The detail of the questionnaire
    included information about prevalence of H. pylori infection, facilities to perform H. pylori culture, molecular testing
    for antibiotic resistance and antibiotic resistance rate in their countries. Results: H. pylori infection remain common
    in ASEAN ranging from 20% in Malaysia, 21-54% in Thailand and 69% in Myanmar. Most of ASEAN countries
    can perform H. pylori cultures and antibiotic susceptibility tests except Laos and Cambodia. In ASEAN countries,
    metronidazole resistant H pylori is quite common whereas amoxicillin resistance remain rare. Clarithromycin resistance
    results in a significant decrease in H. pylori eradication rate with clarithromycin-containing regimens. The prevalence of
    clarithromycin resistance varies in ASEAN countries being high in Vietnam (30%) and Cambodia (43%), moderate to high
    in Singapore (17%) and low in Malaysia (6.8%), Philippine (2%) and Myanmar (0%). In Thailand, clarithromycin
    resistance tends to higher in large cities (14%) than in rural areas (~3.7%). Conclusion: ASEAN countries should
    develop a standard protocol for regular susceptibility testing of H. pylori so that clinicians would be better able to
    choose reliably effective empiric therapies. The wide range of antibiotic resistance in ASEAN countries suggests that
    the preferred first line regimen should be depend on the local antibiotic resistance other than single recommendation.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/isolation & purification
  12. Gunaletchumy SP, Teh X, Khosravi Y, Ramli NS, Chua EG, Kavitha T, et al.
    J Bacteriol, 2012 Oct;194(20):5695-6.
    PMID: 23012278
    Helicobacter pylori is the main bacterial causative agent of gastroduodenal disorders and a risk factor for gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. The draft genomes of 10 closely related H. pylori isolates from the multiracial Malaysian population will provide an insight into the genetic diversity of isolates in Southeast Asia. These isolates were cultured from gastric biopsy samples from patients with functional dyspepsia and gastric cancer. The availability of this genomic information will provide an opportunity for examining the evolution and population structure of H. pylori isolates from Southeast Asia, where the East meets the West.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/isolation & purification
  13. Wan Juhari WK, Md Tamrin NA, Mat Daud MH, Isa HW, Mohd Nasir N, Maran S, et al.
    Hugo J, 2014 Dec;8(1):4.
    PMID: 27090252 DOI: 10.1186/s11568-014-0004-0
    BACKGROUND: The sequencing of two members of the Royal Kelantan Malay family genomes will provide insights on the Kelantan Malay whole genome sequences. The two Kelantan Malay genomes were analyzed for the SNP markers associated with thalassemia and Helicobacter pylori infection. Helicobacter pylori infection was reported to be low prevalence in the north-east as compared to the west coast of the Peninsular Malaysia and beta-thalassemia was known to be one of the most common inherited and genetic disorder in Malaysia.

    RESULT: By combining SNP information from literatures, GWAS study and NCBI ClinVar, 18 unique SNPs were selected for further analysis. From these 18 SNPs, 10 SNPs came from previous study of Helicobacter pylori infection among Malay patients, 6 SNPs were from NCBI ClinVar and 2 SNPs from GWAS studies. The analysis reveals that both Royal Kelantan Malay genomes shared all the 10 SNPs identified by Maran (Single Nucleotide Polymorphims (SNPs) genotypic profiling of Malay patients with and without Helicobacter pylori infection in Kelantan, 2011) and one SNP from GWAS study. In addition, the analysis also reveals that both Royal Kelantan Malay genomes shared 3 SNP markers; HBG1 (rs1061234), HBB (rs1609812) and BCL11A (rs766432) where all three markers were associated with beta-thalassemia.

    CONCLUSIONS: Our findings suggest that the Royal Kelantan Malays carry the SNPs which are associated with protection to Helicobacter pylori infection. In addition they also carry SNPs which are associated with beta-thalassemia. These findings are in line with the findings by other researchers who conducted studies on thalassemia and Helicobacter pylori infection in the non-royal Malay population.

    Matched MeSH terms: Helicobacter pylori
  14. Ontsira Ngoyi EN, Atipo Ibara BI, Moyen R, Ahoui Apendi PC, Ibara JR, Obengui O, et al.
    Helicobacter, 2015 Aug;20(4):316-20.
    PMID: 25585658 DOI: 10.1111/hel.12204
    Helicobacter pylori infection is involved in several gastroduodenal diseases which can be cured by antimicrobial treatment. The aim of this study was to determine the prevalence of H. pylori infection and its bacterial resistance to clarithromycin, fluoroquinolones, and tetracycline in Brazzaville, Congo, by using molecular methods.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/genetics; Helicobacter pylori/isolation & purification
  15. Alfizah H, Ramelah M
    Malays J Pathol, 2012 Jun;34(1):29-34.
    PMID: 22870595 MyJurnal
    Infection with Helicobacter pylori cagA-positive strains is associated with gastroduodenal diseases. The CagA protein is injected into gastric epithelial cells and supposedly induces morphological changes termed the 'hummingbird phenotype', which is associated with scattering and increased cell motility. The molecular mechanisms leading to the CagA-dependent morphological changes are only partially known. The present study was carried out to investigate the effect of CagA variants on the magnitude of gastric epithelial cell morphological changes. Recombinant 3' terminal domains of cagA were cloned and expressed in a gastric epithelial cell line and the hummingbird phenotype was quantified by microscopy. The 3' region of the cagA gene of Malaysian H. pylori isolates showed six sub-genotypes that differed in the structural organization of the EPIYA repeat sequences. The percentage of hummingbird cells induced by CagA increased with duration of transfection. The hummingbird phenotype was observed to be more pronounced when CagA with 4 EPIYA motifs rather than 3 or 2 EPIYA motifs was produced. The activity of different CagA variants in the induction of the hummingbird phenotype in gastric epithelial cells depends at least in part on EPIYA motif variability. The difference in CagA genotypes might influence the potential of individual CagAs to cause morphological changes in host cells. Depending on the relative exposure of cells to CagA genotypes, this may contribute to the various disease outcomes caused by H. pylori infection in different individuals.
    Matched MeSH terms: Helicobacter pylori/classification; Helicobacter pylori/genetics*; Helicobacter pylori/metabolism
  16. Schmidt HM, Goh KL, Fock KM, Hilmi I, Dhamodaran S, Forman D, et al.
    Helicobacter, 2009 Aug;14(4):256-63.
    PMID: 19674129 DOI: 10.1111/j.1523-5378.2009.00684.x
    In vitro studies have shown that the biologic activity of CagA is influenced by the number and class of EPIYA motifs present in its variable region as these motifs correspond to the CagA phosphorylation sites. It has been hypothesized that strains possessing specific combinations of these motifs may be responsible for gastric cancer development. This study investigated the prevalence of cagA and the EPIYA motifs with regard to number, class, and patterns in strains from the three major ethnic groups within the Malaysian and Singaporean populations in relation to disease development.
    Matched MeSH terms: Helicobacter pylori/genetics*; Helicobacter pylori/isolation & purification; Helicobacter pylori/chemistry
  17. Schmidt HM, Andres S, Nilsson C, Kovach Z, Kaakoush NO, Engstrand L, et al.
    Eur J Clin Microbiol Infect Dis, 2010 Apr;29(4):439-51.
    PMID: 20157752 DOI: 10.1007/s10096-010-0881-7
    Helicobacter pylori-related disease is at least partially attributable to the genotype of the infecting strain, particularly the presence of specific virulence factors. We investigated the prevalence of a novel combination of H. pylori virulence factors, including the cag pathogenicity island (PAI), and their association with severe disease in isolates from the three major ethnicities in Malaysia and Singapore, and evaluated whether the cag PAI was intact and functional in vitro. Polymerase chain reaction (PCR) was used to detect dupA, cagA, cagE, cagT, cagL and babA, and to type vacA, the EPIYA motifs, HP0521 alleles and oipA ON status in 159 H. pylori clinical isolates. Twenty-two strains were investigated for IL-8 induction and CagA translocation in vitro. The prevalence of cagA, cagE, cagL, cagT, babA, oipA ON and vacA s1 and i1 was >85%, irrespective of the disease state or ethnicity. The prevalence of dupA and the predominant HP0521 allele and EPIYA motif varied significantly with ethnicity (p < 0.05). A high prevalence of an intact cag PAI was found in all ethnic groups; however, no association was observed between any virulence factor and disease state. The novel association between the HP0521 alleles, EPIYA motifs and host ethnicity indicates that further studies to determine the function of this gene are important.
    Matched MeSH terms: Helicobacter pylori/classification; Helicobacter pylori/genetics*; Helicobacter pylori/isolation & purification*
  18. Mohamed R, Hanafiah A, Rose IM, Manaf MR, Abdullah SA, Sagap I, et al.
    Eur J Clin Microbiol Infect Dis, 2009 Jul;28(7):865-9.
    PMID: 19247698 DOI: 10.1007/s10096-009-0712-x
    We have defined DNA repeat variability in the 3'-terminus of the cagA gene of Helicobacter pylori strains from Malaysian patients of different ethnicities. We identified different alleles based on the EPIYA repeats. cagA types A-B-D and A-B-B-D are more similar to the sequence of Japanese strains, whereas cagA types A-B-C, A-B-C-C, A-B and A-C displayed similarity to strain 26695 sequences. A significant association was found between cagA genotypes and patients' ethnicity, with cagA type A-B-D being predominantly isolated from Chinese patients and cagA type A-B-C from Malays and Indians. Our data further corroborate the possibility that variant biological activity of CagA may affect the host specificity and/or pathogenicity of H. pylori.
    Matched MeSH terms: Helicobacter pylori/classification*; Helicobacter pylori/genetics*; Helicobacter pylori/isolation & purification
  19. Vale FF, Vadivelu J, Oleastro M, Breurec S, Engstrand L, Perets TT, et al.
    Sci Rep, 2015;5:14333.
    PMID: 26387443 DOI: 10.1038/srep14333
    Prophages of Helicobacter pylori, a bacterium known to co-evolve in the stomach of its human host, were recently identified. However, their role in the diversity of H. pylori strains is unknown. We demonstrate here and for the first time that the diversity of the prophage genes offers the ability to distinguish between European populations, and that H. pylori prophages and their host bacteria share a complex evolutionary history. By comparing the phylogenetic trees of two prophage genes (integrase and holin) and the multilocus sequence typing (MLST)-based data obtained for seven housekeeping genes, we observed that the majority of the strains belong to the same phylogeographic group in both trees. Furthermore, we found that the Bayesian analysis of the population structure of the prophage genes identified two H. pylori European populations, hpNEurope and hpSWEurope, while the MLST sequences identified one European population, hpEurope. The population structure analysis of H. pylori prophages was even more discriminative than the traditional MLST-based method for the European population. Prophages are new players to be considered not only to show the diversity of H. pylori strains but also to more sharply define human populations.
    Matched MeSH terms: Helicobacter pylori
  20. Fauzia KA, Miftahussurur M, Syam AF, Waskito LA, Doohan D, Rezkitha YAA, et al.
    Toxins (Basel), 2020 07 24;12(8).
    PMID: 32722296 DOI: 10.3390/toxins12080473
    We evaluated biofilm formation of clinical Helicobacter pylori isolates from Indonesia and its relation to antibiotic resistance. We determined the minimum inhibition concentration (MIC) of amoxicillin, clarithromycin, levofloxacin, metronidazole and tetracycline by the Etest to measure the planktonic susceptibility of 101 H. pylori strains. Biofilms were quantified by the crystal violet method. The minimum biofilm eradication concentration (MBEC) was obtained by measuring the survival of bacteria in a biofilm after exposure to antibiotics. The majority of the strains formed a biofilm (93.1% (94/101)), including weak (75.5%) and strong (24.5%) biofilm-formers. Planktonic resistant and sensitive strains produced relatively equal amounts of biofilms. The resistance proportion, shown by the MBEC measurement, was higher in the strong biofilm group for all antibiotics compared to the weak biofilm group, especially for clarithromycin (p = 0.002). Several cases showed sensitivity by the MIC measurement, but resistance according to the MBEC measurements (amoxicillin, 47.6%; tetracycline, 57.1%; clarithromycin, 19.0%; levofloxacin, 38.1%; and metronidazole 38.1%). Thus, biofilm formation may increase the survival of H. pylori and its resistance to antibiotics. Biofilm-related antibiotic resistance should be evaluated with antibiotic susceptibility.
    Matched MeSH terms: Helicobacter pylori/drug effects*; Helicobacter pylori/isolation & purification; Helicobacter pylori/physiology
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