Response of IgG1 and IgG2 subclasses to Helicobacter pylori in subjects with chronic inflammation of the gastric mucosa, atrophy and gastric cancer in a country with high Helicobacter pylori infection prevalence.
Polarized immune response to Helicobacter pylori and induction of chronic inflammation may increase the risk of gastric atrophy and adenocarcinoma. We studied the association of the response of IgG1 and IgG2 antibodies to H. pylori with grade of gastric chronic inflammation and atrophy in a population with a high prevalence of H. pylori, and compared these data with the data obtained from the study of gastric cancer patients, as well as with the data for CagA positivity. Altogether, 114 persons from two adult population samples from Estonia and 45 consecutive gastric cancer patients were studied. All patients were positive for the H. pylori antibody determined by ELISA. Adenocarcinoma was classified histologically according to the Laurén's system. The response of the IgG subclasses to H. pylori (acid glycine-extracted whole cell proteins) was determined by ELISA and the results were compared with the ELISA results for the recombinant fragment of the CagA protein. Helicobacter pylori IgG level was lower in atrophic gastritis compared with nonatrophic gastritis (chronic inflammation) (p=0.001). In the group of cancer patients, the response of IgG and IgG1 was lower compared with both gastritis groups (p=0.01 and p=0.0002 for IgG, and p=0.001 and p=0.0005 for IgG1). IgG2 was lower for gastric cancer localized in the corpus (p=0.03). In conclusion, atrophic gastritis and gastric cancer were associated with a significant decline in IgG and IgG1 response to H. pylori compared with nonatrophic gastritis. Higher value of CagA antibodies was seen in gastric cancer and in gastric atrophy compared with nonatrophic gastritis; in gastric cancer patients, IgG1 response to H. pylori was correlated with CagA status.
Vorobjova
Tamara
T
Centre of Molecular and Clinical Medicine, Institute of General and Molecular Pathology, University of Tartu, Tartu, Estonia. tamara.vorobjova@kliinikum.ee
Ren
Zhigang
Z
Dunkley
Margaret
M
Clancy
Robert
R
Maaroos
Heidi-Ingrid
HI
Labotkin
Rait
R
Kull
Karl
K
Uibo
Raivo
R
D000230:Adenocarcinoma / Q000097:blood* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000378:metabolism; D001426:Bacterial Proteins / Q000378:metabolism; D001706:Biopsy; D004957:Estonia; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology; D005756:Gastritis / Q000097:blood* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D005757:Gastritis, Atrophic / Q000097:blood / Q000378:metabolism / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori / Q000276:immunology*; D006785:Hospitals, University; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007249:Inflammation / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D013274:Stomach Neoplasms / Q000097:blood* / Q000209:etiology / Q000378:metabolism / Q000473:pathology
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D007074:Immunoglobulin G; C080866:cagA protein, Helicobacter pylori