64 research outputs found
Higher number of Helicobacter pylori CagA EPIYA C phosphorylation sites increases the risk of gastric cancer, but not duodenal ulcer
<p>Abstract</p> <p>Background</p> <p><it>Helicobacter pylori </it>infection is one of the most common infections worldwide and is associated with gastric cancer and peptic ulcer. Bacterial virulence factors such as CagA have been shown to increase the risk of both diseases. Studies have suggested a causal role for CagA EPIYA polymorphisms in gastric carcinogenesis, and it has been shown to be geographically diverse. We studied associations between <it>H. pylori </it>CagA EPIYA patterns and gastric cancer and duodenal ulcer, in an ethnically admixed Western population from Brazil. CagA EPIYA was determined by PCR and confirmed by sequencing. A total of 436 patients were included, being 188 with gastric cancer, 112 with duodenal ulcer and 136 with gastritis.</p> <p>Results</p> <p>The number of EPIYA C segments was significantly associated with the increased risk of gastric carcinoma (OR = 3.08, 95% CI = 1.74 to 5.45, p < 10<sup>-3</sup>) even after adjustment for age and gender. Higher number of EPIYA C segments was also associated with gastric atrophy (p = 0.04) and intestinal metaplasia (p = 0.007). Furthermore, patients infected by <it>cag</it>A strains possessing more than one EPIYA C segment showed decreased serum levels of pepsinogen I in comparison with those infected by strains containing one or less EPIYA C repeat. Otherwise, the number of EPIYA C segments did not associate with duodenal ulcer.</p> <p>Conclusions</p> <p>Our results demonstrate that infection with <it>H. pylori </it>strains harbouring more than one CagA EPIYA C motif was clearly associated with gastric cancer, but not with duodenal ulcer.</p> <p>Higher number of EPIYA C segments was also associated with gastric precancerous lesions as demonstrated by histological gastric atrophic and metaplastic changes and decreased serum levels of pepsinogen I.</p
A 500-year tale of co-evolution, adaptation, and virulence: Helicobacter pylori in the Americas
Helicobacter pylori is a common component of the human stomach microbiota, possibly dating back to the speciation of Homo sapiens. A history of pathogen evolution in allopatry has led to the development of genetically distinct H. pylori subpopulations, associated with different human populations, and more recent admixture among H. pylori subpopulations can provide information about human migrations. However, little is known about the degree to which some H. pylori genes are conserved in the face of admixture, potentially indicating host adaptation, or how virulence genes spread among different populations. We analyzed H. pylori genomes from 14 countries in the Americas, strains from the Iberian Peninsula, and public genomes from Europe, Africa, and Asia, to investigate how admixture varies across different regions and gene families. Whole-genome analyses of 723 H. pylori strains from around the world showed evidence of frequent admixture in the American strains with a complex mosaic of contributions from H. pylori populations originating in the Americas as well as other continents. Despite the complex admixture, distinctive genomic fingerprints were identified for each region, revealing novel American H. pylori subpopulations. A pan-genome Fst analysis showed that variation in virulence genes had the strongest fixation in America, compared with non-American populations, and that much of the variation constituted non-synonymous substitutions in functional domains. Network analyses suggest that these virulence genes have followed unique evolutionary paths in the American populations, spreading into different genetic backgrounds, potentially contributing to the high risk of gastric cancer in the region.Fil: Muñoz Ramirez, Zilia Y.. INSTITUTO POLITĂCNICO NACIONAL (IPN);Fil: Pascoe, Ben. University of Bath; Reino UnidoFil: Mendez Tenorio, Alfonso. INSTITUTO POLITĂCNICO NACIONAL (IPN);Fil: Mourkas, Evangelos. University of Bath; Reino UnidoFil: Sandoval Motta, Santiago. Consejo Nacional de Ciencia y TecnologĂa; MĂ©xicoFil: Perez Perez, Guillermo. New York University Langone Medical Center; Estados UnidosFil: Morgan, Douglas R.. University of Alabama at Birmingahm; Estados UnidosFil: Dominguez, Ricardo Leonel. Western Honduras Gastric Cancer Prevention Initiative Hospital de Occidente Santa Rosa de Copan; HondurasFil: Ortiz Princz, Diana. No especifĂca;Fil: Cavazza, Maria Eugenia. No especifĂca;Fil: Rocha, Gifone. Universidade Federal de Minas Gerais; BrasilFil: Queiroz, Dulcienne. Universidade Federal de Minas Gerais; BrasilFil: Catalano, Mariana. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de Investigaciones en MicrobiologĂa y ParasitologĂa MĂ©dica. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones en MicrobiologĂa y ParasitologĂa MĂ©dica; ArgentinaFil: Zerbetto de Palma, Gerardo Gabriel. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de QuĂmica y FĂsico-QuĂmica BiolĂłgicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y BioquĂmica. Instituto de QuĂmica y FĂsico-QuĂmica BiolĂłgicas; ArgentinaFil: Goldman, Cinthia Gabriela. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y BioquĂmica; ArgentinaFil: Venegas, Alejandro. Universidad Diego Portales; ChileFil: Alarcon, Teresa. Universidad AutĂłnoma de Madrid; EspañaFil: Oleastro, Monica. Universidade Nova de Lisboa; PortugalFil: Vale, Filipa F.. Universidade Nova de Lisboa; PortugalFil: Goodman, Karen J.. University of Alberta; CanadĂĄFil: Torres, Roberto C.. Instituto Mexicano del Seguro Social; MĂ©xicoFil: Berthenet, Elvire. Swansea University Medical School; Reino UnidoFil: Hitchings, Matthew D.. Swansea University Medical School; Reino UnidoFil: Blaser, Martin J.. Rutgers University; Estados UnidosFil: Sheppard, Samuel K.. University of Bath; Reino UnidoFil: Thorell, Kaisa. University of Gothenburg; SueciaFil: Torres, Javier. Instituto Mexicano del Seguro Social; MĂ©xic
Helicobacter pylori infection in infants and toddlers in South America: concordance between [ÂčÂłC] urea breath test and monoclonal H. pylori stool antigen test
Accurate noninvasive tests for diagnosing Helicobacter pylori infection in very young children are strongly required. We investigated the agreement between the [ÂčÂłC] urea breath test ([ÂčÂłC]UBT) and a monoclonal ELISA (HpSA) for detection of H. pylori antigen in stool. From October 2007 to July 2011, we enrolled 414 infants (123 from Brazil and 291 from Peru) of ages 6 to 30 months. Breath and stool samples were obtained at intervals of at least 3 months from Brazilian (n = 415) and Peruvian (n = 908) infants. [ÂčÂłC]UBT and stool test results concurred with each other in 1,255 (94.86%) cases (kappa coefficient = 0.90; 95% confidence interval [CI] = 0.87 to 0.92). In the H. pylori-positive group, delta-over-baseline (DOB) and optical density (OD) values were positively correlated (r = 0.62; P < 0.001). The positivity of the tests was higher (P < 0.001; odds ratio [OR] = 6.01; 95% CI = 4.50 to 8.04) in Peru (546/878; 62.2%) than in Brazil (81/377; 21.5%) and increased with increasing age in Brazil (P = 0.02), whereas in Peru it decreased with increasing age (P < 0.001). The disagreement between the test results was associated with birth in Brazil and female gender but not with age and diarrhea. Our results suggest that both [ÂčÂłC]UBT and the stool monoclonal test are reliable for diagnosing H. pylori infection in very young children, which will facilitate robust epidemiological studies in infants and toddlers
Immunoblotting for the serodiagnosis of Helicobacter pylori  infection in Brazilian patients with and without gastric carcinoma
Iron status and Helicobacter pylori infection in symptomatic children: an international multi-centered study
Objective:Iron deficiency (ID) and iron deficiency anaemia (IDA) are global major public health problems, particularly in developing countries. Whilst an association between H. pylori infection and ID/IDA has been proposed in the literature, currently there is no consensus. We studied the effects of H. pylori infection on ID/IDA in a cohort of children undergoing upper gastrointestinal endoscopy for upper abdominal pain in two developing and one developed country.Methods:In total 311 children (mean age 10.7±3.2 years) from Latin America - Belo Horizonte/Brazil (n = 125), Santiago/Chile (n = 105) - and London/UK (n = 81), were studied. Gastric and duodenal biopsies were obtained for evaluation of histology and H. pylori status and blood samples for parameters of ID/IDA.Results:The prevalence of H. pylori infection was 27.7% being significantly higher (p<0.001) in Latin America (35%) than in UK (7%). Multiple linear regression models revealed H. pylori infection as a significant predictor of low ferritin and haemoglobin concentrations in children from Latin-America. A negative correlation was observed between MCV (r = -0.26; p = 0.01) and MCH (r = -0.27; p = 0.01) values and the degree of antral chronic inflammation, and between MCH and the degree of corpus chronic (r = -0.29, p = 0.008) and active (r = -0.27, p = 0.002) inflammation.Conclusions:This study demonstrates that H. pylori infection in children influences the serum ferritin and haemoglobin concentrations, markers of early depletion of iron stores and anaemia respectively
Depression rather than liver impairment reduces quality of life in patients with hepatitis C
Accuracy of a Commercial Enzyme-Linked Immunosorbent Assay for CagA in Patients from Brazil with and without Gastric Carcinoma
We validated a commercial enzyme-linked immunosorbent assay for the detection of anti-CagA antibodies in Brazilian patients with Helicobacter pylori infection. The test presented high sensitivity (97.4%) and specificity (88.9%) when employed in patients without gastric carcinoma. However, in gastric carcinoma patients, the test was neither sensitive nor specific enough to detect cagA-positive H. pylori infection
Su1651 A New Variant of H. pylori vacA is Associated With Precancerous Lesions and Gastric Cancer
S1643 The Higher Number of EPIYA-C Segments of the H. pylori cagA Protein is a Risk Factor for Gastric Cancer and the Eastern cagA-Multimerization (CM) Sequence is Associated With Tumor Diffuse Type
T1637 Gastric Carcinoma Patients Have a Specific Cytokine Profile Characterized By Strongly Increased Levels of Treg Cytokines, IL-1ÎČ, IL-6, IL-8 and IL-23 and Decreased Levels of IL-1α, IL-12p70, IFN-Îł and TNF-α
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