{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T10:29:07Z","timestamp":1761560947548},"reference-count":13,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2005,2,1]],"date-time":"2005-02-01T00:00:00Z","timestamp":1107216000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Clin Vaccine Immunol"],"published-print":{"date-parts":[[2005,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            CagA seropositivity is an important risk factor for gastric adenocarcinoma and duodenal ulcer. However, CagA seropositivity is also found in\n            <jats:italic>Helicobacter pylori<\/jats:italic>\n            -seronegative subjects. Is CagA seropositivity in these subjects a sign of a past\n            <jats:italic>H. pylori<\/jats:italic>\n            infection, or does it represent a false-positive reaction? This study investigates the intensity of the CagA immune reaction and the variation in CagA seroprevalence with year of birth for 650 subjects belonging to the Malmo\u0308 Preventive Medicine cohort. CagA and\n            <jats:italic>H. pylori<\/jats:italic>\n            seroprevalences were determined by Western blot analysis (Helicoblot 2.1) and enzyme-linked immunosorbent assay. The peak intensity of the CagA band was significantly lower in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seronegative subjects than in those with concomitant\n            <jats:italic>H. pylori<\/jats:italic>\n            seropositivity. In\n            <jats:italic>H. pylori<\/jats:italic>\n            -seropositive subjects, peak CagA intensity had a bimodal distribution. The prevalence of CagA-seropositive but\n            <jats:italic>H. pylori<\/jats:italic>\n            -seronegative subjects increased successively and significantly with year of birth, in contrast to the prevalence of CagA-seropositive and\n            <jats:italic>H. pylori<\/jats:italic>\n            -seropositive subjects, which decreased significantly. However, within\n            <jats:italic>H. pylori<\/jats:italic>\n            -seropositive and -seronegative subgroups, CagA seroprevalences were constant for different birth cohorts. If CagA seropositivity in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seronegative subjects represents a past\n            <jats:italic>H. pylori<\/jats:italic>\n            infection, there must have been some mechanisms of eradication that were more common in younger subjects and that were of more importance than the presence of gastric atrophy and the longer duration and higher prevalence of\n            <jats:italic>H. pylori<\/jats:italic>\n            infection found in older subjects. Antibiotic treatment of\n            <jats:italic>H. pylori<\/jats:italic>\n            was not common practice at the time of enrollment. On the other hand, a false-positive reaction would be constant and independent of birth cohorts, as with the\n            <jats:italic>H. pylori<\/jats:italic>\n            -seronegative subgroup of our study. Peak CagA intensity in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seronegative subjects corresponded to the lower part of the bimodal distribution of peak CagA intensity in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seropositive subjects. We conclude that a major proportion of CagA seropositivity in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seronegative subjects represents a false-positive reaction. Peak CagA intensity has a bimodal distribution in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seropositive subjects. Low-intensity CagA seropositivity in\n            <jats:italic>H. pylori<\/jats:italic>\n            -seropositive subjects is indeterminate, representing both false-positive and true-positive reactions.\n          <\/jats:p>","DOI":"10.1128\/cdli.12.2.304-309.2005","type":"journal-article","created":{"date-parts":[[2005,2,7]],"date-time":"2005-02-07T22:28:47Z","timestamp":1107815327000},"page":"304-309","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Evaluation of Western Blot CagA Seropositivity in\n            <i>Helicobacter pylori<\/i>\n            -Seropositive and -Seronegative Subjects"],"prefix":"10.1128","volume":"12","author":[{"given":"J. Henrik","family":"Sima\u0301n","sequence":"first","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Medical Microbiology, Malmo\u0308 University Hospital, Lund University, Malmo\u0308"},{"name":"Department of Medical Epidemiology, Karolinska Institutet, Stockholm"},{"name":"Department of Medicine, Lund University Hospital, Lund University, Lund, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lars","family":"Engstrand","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Medical Microbiology, Malmo\u0308 University Hospital, Lund University, Malmo\u0308"},{"name":"Department of Medical Epidemiology, Karolinska Institutet, Stockholm"},{"name":"Department of Medicine, Lund University Hospital, Lund University, Lund, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Go\u0308ran","family":"Berglund","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Medical Microbiology, Malmo\u0308 University Hospital, Lund University, Malmo\u0308"},{"name":"Department of Medical Epidemiology, Karolinska Institutet, Stockholm"},{"name":"Department of Medicine, Lund University Hospital, Lund University, Lund, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Claes-Henrik","family":"Flore\u0301n","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Medical Microbiology, Malmo\u0308 University Hospital, Lund University, Malmo\u0308"},{"name":"Department of Medical Epidemiology, Karolinska Institutet, Stockholm"},{"name":"Department of Medicine, Lund University Hospital, Lund University, Lund, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arne","family":"Forsgren","sequence":"additional","affiliation":[{"name":"Department of Medicine"},{"name":"Department of Medical Microbiology, Malmo\u0308 University Hospital, Lund University, Malmo\u0308"},{"name":"Department of Medical Epidemiology, Karolinska Institutet, Stockholm"},{"name":"Department of Medicine, Lund University Hospital, Lund University, Lund, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"2111","volume":"55","year":"1995","unstructured":"Blaser, M. J., G. I. Perez-Perez, H. Kleanthous, T. L. Cover, R. M. Peek, P. H. Chyou, G. N. Stemmermann, and A. Nomura. 1995. Infection with Helicobacter pylori strains possessing cagA is associated with an increased risk of developing adenocarcinoma of the stomach. Cancer Res.55:2111-2115.","journal-title":"Cancer Res."},{"key":"e_1_3_2_3_2","doi-asserted-by":"crossref","first-page":"446","DOI":"10.1002\/ijc.10201","volume":"98","year":"2002","unstructured":"Brenner, H., V. Arndt, G. Bode, C. Stegmaier, H. Ziegler, and T. St\u00fcmer. 2002. Risk of gastric cancer among smokers infected with Helicobacter pylori. Int. J. Cancer98:446-449.","journal-title":"Int. J. Cancer"},{"key":"e_1_3_2_4_2","doi-asserted-by":"crossref","first-page":"784","DOI":"10.1053\/gast.2001.27999","volume":"121","year":"2001","unstructured":"Ekstr\u00f6m, A. M., M. Held, L. E. Hansson, L. Engstrand, and O. Nyr\u00e9n. 2001. 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P\u00e9rez-P\u00e9rez, J. Lee, G. Stemmermann, and M. J. Blaser. 2002. Relation between Helicobacter pylori cagA status and risk of peptic ulcer disease. Am. J. Epidemiol.155:1054-1059.","journal-title":"Am. J. Epidemiol."},{"key":"e_1_3_2_11_2","doi-asserted-by":"crossref","first-page":"297","DOI":"10.1136\/gut.40.3.297","volume":"40","year":"1997","unstructured":"Parsonnet, J., G. D. Friedman, N. Orentreich, and H. Vogelman. 1997. Risk for gastric cancer in people with CagA positive or CagA negative Helicobacter pylori infection. Gut40:297-301.","journal-title":"Gut"},{"key":"e_1_3_2_12_2","doi-asserted-by":"crossref","first-page":"1215","DOI":"10.3109\/00365529709028150","volume":"32","year":"1997","unstructured":"Sim\u00e1n, J. H., A. Forsgren, G. Berglund, and C. H. Flor\u00e9n. 1997. Association between Helicobacter pylori and gastric carcinoma in the city of Malm\u00f6, Sweden. A prospective study. Scand. J. Gastroenterol.32:1215-1221.","journal-title":"A prospective study. Scand. J. Gastroenterol."},{"key":"e_1_3_2_13_2","doi-asserted-by":"crossref","first-page":"147","DOI":"10.3109\/00365549709035875","volume":"29","year":"1997","unstructured":"Sorberg, M., L. Engstrand, M. Strom, K. A. Jonsson, H. Jorbeck, and M. Granstrom. 1997. The diagnostic value of enzyme immunoassay and immunoblot in monitoring eradication of Helicobacter pylori. Scand. J. Infect. Dis.29:147-151.","journal-title":"Scand. J. Infect. Dis."},{"key":"e_1_3_2_14_2","doi-asserted-by":"crossref","first-page":"497","DOI":"10.1046\/j.1365-2036.2002.01197.x","volume":"16","year":"2002","unstructured":"Stack, W. A., J. C. Atherton, G. M. Hawkey, R. F. Logan, and C. J. Hawkey. 2002. Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding. Aliment. Pharmacol. Ther.16:497-506.","journal-title":"Aliment. Pharmacol. 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