Serologic IgG recognition of Helicobacter pylori cytotoxin-associated protein, peptic ulcer and gastroduodenal pathology in childhood

Oderda, Giuseppina; Figura, Natale; Bayeli, P. F.; Basagni, C; Bugnoli, M; Armellini, D.; Altare, F; Ansaldi, N

doi:10.1097/00042737-199309000-00005

Cited by 33 publications

(26 citation statements)

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“…The variation in frequency of such diseases may in part depend on differences in cytotoxin production and possession of the cag A gene by H pylori 46 9 10 12 13 Most studies on the pathogenic potential of these factors have been carried out by examining only one colony, or pooled colonies, of H pylori per patient on a single occasion, or by determining the local or the systemic immune response to the vacuolating toxin or the CagA protein. However, seropositivity for VacA and CagA does not determine the composition of the bacterial population in the stomach, and the characteristics of a single clone cannot be extrapolated to all the helicobacters colonising the same organ.…”

Section: Discussionmentioning

confidence: 99%

cagA positive and negative Helicobacter pyloristrains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

Figura

Vindigni

Covacci

et al. 1998

Gut

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Background/Aims-Infection with Helicobacter pylori strains harbouring the cagA gene (cagA+) is associated with an increased risk of developing peptic ulcer and gastric cancer. The aim of this study was to assess whether H pylori isolates with diVerent cagA status were present in patients with non-ulcer dyspepsia, and whether a variable cagA status is relevant to histological gastric mucosal damage and glandular cell proliferation. Methods-Well separated H pylori colonies (between 2 and 25) from primary plates, per gastric area, for each of 19 patients with non-ulcer dyspepsia were examined for cagA by hybridisation. Western blotting was used to examine both representative colonies for CagA expression and the patients' sera for antibody response to CagA. Glandular gastric cell proliferation was assessed immunohistochemically. Results-Of the 747 colonies examined, 45.3% were cagA+. All colonies from four patients were cagA+, and all colonies from two patients were cagA−. In 13 patients (68%) both cagA+ and cagA− colonies were found. CagA expression of isolates corresponded to their cagA status. H pylori strains with diVerent CagA molecular masses were present in three patients. Results based on all 19 patients studied showed that the prevalence of cagA+ colonies in areas with mucosal atrophy associated or not with intestinal metaplasia (67.9%) was significantly higher than in normal mucosa (44.7%) and mucosa from patients with chronic gastritis (44.0%) (p< 0.001). High levels of cell proliferation were associated with histological atrophy with or without intestinal metaplasia, but not with the possession of cagA by organisms colonising the same mucosal sites. Conclusions-Most patients with nonulcer dyspepsia are infected by both cagA+ and cagA− H pylori colonies. The cagA status of infecting organisms may play a role in the development of atrophy and intestinal metaplasia. (Gut 1998;42:772-778)

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Section: Discussionmentioning

confidence: 99%

cagA positive and negative Helicobacter pyloristrains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

Figura

Vindigni

Covacci

et al. 1998

Gut

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“…H. pylori strains that express the cagA protein are endowed with increased pathogenicity. Studies have shown that the prevalence of antibodies to the cagA protein is higher in patients with peptic ulcer disease than in H. pylori gastritis without ulcer [16][17][18][19]. However it is not clear if increased titres of CagA antibodies are associated with an increased eosinophil and mast cell infiltration.…”

Section: Introductionmentioning

confidence: 99%

The role of mast cells and eosinophils in chronic gastritis

et al. 2006

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The role of mast cells and eosinophils in influencing the pathology of chronic gastritis remains unclear. We attempted to study the relationship between endoscopy and the mast cell and eosinophil infiltrate. We also studied the role of gene polymorphisms, Helicobacter pylori density and the CagA antibody status in influencing the mast cell and eosinophil infiltrate. One hundred and twenty consecutive patients were studied. Endoscopic evaluation was done and 3 antral biopsies were taken from each patient and were assessed for eosinophilic and mast cell infiltration, H. pylori density and the density of the other inflammatory cells as per the revised Sydney system. Cytokine gene polymorphisms (IL-1beta, IL-1RA and TNF-alpha) were done on the DNA extracted from the peripheral blood by PCR-RFLP. ELISA was done on the patients' serum for the anti-CagA antibody titres. Nodularity is strongly associated with the presence and density of eosinophils on biopsy (P < 0.05). Eosinophil density is strongly associated with the density of H. pylori, neutrophils, lymphocytes, plasma cells, atrophy, ulceration, foveolitis and lymphoid follicles. The mast cell density is not associated with any of the other histopathological variables. Gene polymorphisms and the CagA antibody titres have no relationship to the mast cell and eosinophil density. Eighty-one patients showed positive anti-CagA antibody titres but there was no association with the eosinophilic or the mast cell infiltrate. It is likely that eosinophilic infiltration is influenced by the H. pylori density but the CagA protein has no role to play in influencing the grade of the eosinophilic infiltrate in the Indian context. Cytokine gene proinflammatory polymorphisms have no role to play in influencing the eosinophilic or the mast cell response. It is likely that other mediators are involved in the inflammatory cell responses.

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“…IL-8 is a powerful chemotactic factor and an activator of polymorphonuclear leukocytes and macrophages, contributing to a stronger inflammatory response in patients colonized by cag-PAIpositive strains. Therefore, patients infected by cagApositive strains have larger bacterial density in the gastric mucosa, more severe epithelial injury, more intense polymorphonuclear leukocyte infiltration, and higher levels of proinflammatory cytokines, which endorses the commonly reported association between infection by cagA-positive strains and peptic ulcer disease in children 45,46 and adults, 6,7,47 or gastric carcinoma in adults. [48][49][50] In Brazil, 95.0 and 62.3% of strains isolated from children with and without duodenal ulcer, respectively, are cagApositive.…”

Section: Gastroenterology Of Hospital Das Clínicas Of Universidadementioning

confidence: 55%

Úlcera péptica gastroduodenal e infecção pelo Helicobacter pylori na criança e adolescente

Bittencourt¹,

Rocha²,

Penna³

et al. 2006

J. Pediatr. (Rio J.)

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Objective: To show important aspects of gastroduodenal peptic ulcer and of Helicobacter pylori infection in children and adolescents. Sources: Technical textbooks and MEDLINE and LILACS databases including publications between 1966 and 2006.Summary of the findings: The etiology of peptic ulcer in children and adolescents may be primary, associated with H. pylori infection, or secondary, in which etiopathogenic mechanisms rely upon the underlying disease. The infection is acquired predominantly in childhood, with prevalence rates between 56.8 and 83.1% in children who live in the poorest Brazilian regions, amounting to nearly 10% in children aged less than 10 years in industrialized countries. The infection can be diagnosed by invasive methods, which investigate the presence of the bacterium, or of DNA, RNA or bacterial products in biopsy fragments of the gastric mucosa obtained at endoscopic examination; it can also be diagnosed through noninvasive methods, which include the detection of anti-H. pylori antibodies in serum, urine or saliva samples, detection of bacterial antigens in stool samples, and the carbon 13-labeled urea breath test. However, upper gastrointestinal endoscopy is the method of choice for the diagnosis of peptic ulcer, as it allows collecting fragments from the gastric mucosa during the procedure for the diagnosis of infection and for histopathological analysis.Conclusions: H. pylori infection is the major cause of peptic ulcer among children. Eradication of the bacterium with antimicrobial therapy results in the cure of the disease, and is therefore indicated for all children with H. pylori infection with an active, recurrent, healed, or complicated peptic ulcer.

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Serologic IgG recognition of Helicobacter pylori cytotoxin-associated protein, peptic ulcer and gastroduodenal pathology in childhood

Cited by 33 publications

References 0 publications

cagA positive and negative Helicobacter pyloristrains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

cagA positive and negative Helicobacter pyloristrains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage

The role of mast cells and eosinophils in chronic gastritis

Úlcera péptica gastroduodenal e infecção pelo Helicobacter pylori na criança e adolescente

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