Phenotypic diversity in Lewis expression of Helicobacter pylori isolates from the same host

Wirth, H; Yang, Muwen; Peek, Richard M.; Höök‐Nikanne, Johanna; Fried, Michael; Blaser, Martin J.

doi:10.1016/s0022-2143(99)90026-4

Cited by 69 publications

(61 citation statements)

References 36 publications

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“…The variability observed in the expression of Le antigen was not due to colonization with different strains, since in seven of the eight patients all of the isolated colonies showed the same RAPD pattern, and only in one case (patient 259) was a mixed infection documented, showing two different RAPD patterns. In accordance with these results, a previous study also reported a high diversity in the expression of Le antigens among multiple isolates from single patients even if they had the same RAPD pattern; the authors of that study suggested that variability in expression of Le antigens is not due to genetic diversity but to mechanisms regulating the expression and activity of fucosyltransferases (11). This variability would justify considering each colony as a phenotypically independent event for the statistical analyses.…”

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confidence: 71%

Lewis Antigen Expression by Helicobacter pylori Strains Colonizing Different Regions of the Stomach of Individual Patients

et al. 2008

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confidence: 71%

Lewis Antigen Expression by Helicobacter pylori Strains Colonizing Different Regions of the Stomach of Individual Patients

et al. 2008

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“…First, humans may simultaneously carry both cag ϩ and cag-negative strains, and if only a single colony is used as the basis to determine cag presence, this may represent a false-negative result (18,20,49,53). Second, even among persons known to carry cag ϩ strains, there may be a spontaneous loss of cagA and other parts of the cag island (53,57). Third, sequence heterogeneity and technical limitations may compromise PCR methodologies (54).…”

Section: Discussionmentioning

confidence: 99%

Local and Systemic Immune and Inflammatory Responses to Helicobacter pylori Strains

Bhat

Gaensbauer

Peek

et al. 2005

Clin Vaccine Immunol

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Colonization with Helicobacter pylori eventuates in varied clinical outcomes, which relate to both bacterial and host factors. Here we examine the relationships between cagA status, serum and gastric juice antibody responses, and gastric inflammation in dyspeptic patients. Serum, gastric juice, and gastric biopsy specimens were obtained from 89 patients undergoing endoscopy. H. pylori colonization and cagA status were determined by histology, culture, and PCR methods, and acute inflammation and chronic inflammation in the gastric mucosa were scored by a single pathologist. Serum and gastric juice antibodies to H. pylori whole-cell and CagA antigens were determined by enzyme-linked immunosorbent assay. Relationships between variables were sequentially analyzed using univariate and multivariate statistical methods. Of the 89 subjects, 62 were colonized by H. pylori. By univariate analyses, levels of serum immunoglobulin G (IgG) and IgA and gastric juice IgA antibodies against whole-cell and CagA antigens each were significantly higher in the H. pyloripositive group than in the H. pylori-negative group (P < 0.001). H. pylori and CagA seropositivities were both significantly associated with enhanced inflammation in gastric antrum and body (P < 0.02). The presence of gastric juice antibodies to H. pylori antigens was associated with more severe gastric inflammation. However, in multivariate analyses, only the presence of serum antibodies against CagA and, to a lesser extent, whole-cell antigens remained significantly associated with acute and chronic inflammation in antrum and body (P < 0.05). Thus, serum antibody response to CagA correlates with severity of gastric inflammation. Furthermore, given the relationships demonstrated by multivariate analysis, determination of gastric juice antibodies may provide a better representation of serum, rather than secretory, immune response.

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“…Little work on in vivo gene expression of H. pylori has been done, but transcript levels of four important Helicobacter genes are similar for human biopsy samples and mouse samples (23). However, there is no detectable phase variation of Lewis antigen expression (27), and the important virulence factors CagA and VacA are lost during mouse colonization (11,25). Pathological changes in the murine system include gastritis and in some cases follicle formation and even lowgrade mucosa-associated lymphoid tissue lymphoma in the gastric mucosa (5,17), whereas ulcer formation and adenocarcinoma have not been observed.…”

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A Comparison of Murine and Human Immunoproteomes of Helicobacter pylori Validates the Preclinical Murine Infection Model for Antigen Screening

Bumann¹,

Holland²,

Siejak

et al. 2002

Infect Immun

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Preclinical mouse infection models are widely used for Helicobacter vaccine development, but how well such models mimic important aspects of human infections is unknown. A comparison of Helicobacter pylori immunoproteomes of infected mice with previously reported patient data reveals a high agreement in the antigens recognized, suggesting that H. pylori in vivo protein composition and recognition by the host immune system are comparable in mice and humans. Murine Helicobacter models may thus be valid to screen antigens for human vaccination.

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Phenotypic diversity in Lewis expression of Helicobacter pylori isolates from the same host

Cited by 69 publications

References 36 publications

Lewis Antigen Expression by Helicobacter pylori Strains Colonizing Different Regions of the Stomach of Individual Patients

Lewis Antigen Expression by Helicobacter pylori Strains Colonizing Different Regions of the Stomach of Individual Patients

Local and Systemic Immune and Inflammatory Responses to Helicobacter pylori Strains

A Comparison of Murine and Human Immunoproteomes of Helicobacter pylori Validates the Preclinical Murine Infection Model for Antigen Screening

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