Aim of this study is to provide indirect evidence that human colonie inucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopie biopsies from 26 patients and in rectal samples of a further 36. AH had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810±0.668 optical density vs 0329+0.509 optical density for IgG, p=0.007 and 0.660±0.477 vs 0.116±0.229 for IgA, p<0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p=0.16) different between Helicobacter pylori positive (48/62, 77%; 0.243±0.388 optical density) and negative (14/62, 23%; 0.095±0.088) patients. In same material, levels of Helicobacter pylori IgA were very low or undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.

Evidence against colonie mucosa colonisation by Helicobacter pylori. Lack of a specific antibody response in homogenates of rectal endoscopie biopsies

Luzza F.;
1996-01-01

Abstract

Aim of this study is to provide indirect evidence that human colonie inucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopie biopsies from 26 patients and in rectal samples of a further 36. AH had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810±0.668 optical density vs 0329+0.509 optical density for IgG, p=0.007 and 0.660±0.477 vs 0.116±0.229 for IgA, p<0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p=0.16) different between Helicobacter pylori positive (48/62, 77%; 0.243±0.388 optical density) and negative (14/62, 23%; 0.095±0.088) patients. In same material, levels of Helicobacter pylori IgA were very low or undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.
1996
Gastric homogenate
Helicobacter pylori
Immunoglobulin a
Immunoglobulin g
Rectal homogenate
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12317/63511
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