{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T04:04:51Z","timestamp":1778558691993,"version":"3.51.4"},"reference-count":29,"publisher":"BMJ","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"accepted":{"date-parts":[[1997,3,10]]},"published-print":{"date-parts":[[1997,10,1]]},"abstract":"<jats:p>\n                    <jats:italic>Background<\/jats:italic>\n                    <jats:italic>\u2014Helicobacter pylori<\/jats:italic>\n                    strains possessing the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene and the expression patterns of cytokines other than IL-8.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Aims<\/jats:italic>\n                    <jats:italic>\u2014<\/jats:italic>\n                    To investigate the relation between the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Patients and methods<\/jats:italic>\n                    <jats:italic>\u2014<\/jats:italic>\n                    In 184 patients, the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1\u03b2, IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor \u03b1 (TNF-\u03b1) in antral biopsy specimens were measured by ELISA.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Results\u2014<\/jats:italic>\n                    Mucosal levels of IL-1\u03b2, IL-6, IL-8, and TNF-\u03b1 were significantly higher in\n                    <jats:italic>H pylori<\/jats:italic>\n                    positive than in\n                    <jats:italic>H pylori<\/jats:italic>\n                    negative patients. Furthermore, the mucosal levels of IL-1\u03b2 and IL-8 were significantly higher in specimens infected with\n                    <jats:italic>cagA<\/jats:italic>\n                    positive strains than in those infected with\n                    <jats:italic>cagA<\/jats:italic>\n                    negative strains. In\n                    <jats:italic>H pylori<\/jats:italic>\n                    positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1\u03b2 (p&lt;0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-\u03b1 (p&lt;0.0001).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:italic>Conclusion\u2014<\/jats:italic>\n                    These findings suggest that the ability to induce cytokines differs among the strains;\n                    <jats:italic>cagA<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    strains induce various kinds of cytokines and may cause severe inflammation, whereas\n                    <jats:italic>cagA<\/jats:italic>\n                    <jats:sup>\u2212<\/jats:sup>\n                    strains induce IL-8 and IL-1\u03b2 only weakly and may cause only mild inflammation. However, as most patients infected with the\n                    <jats:italic>cagA<\/jats:italic>\n                    <jats:sup>+<\/jats:sup>\n                    strains have gastritis, these strains may not be equivalent to ulcerogenic strains.\n                  <\/jats:p>","DOI":"10.1136\/gut.41.4.442","type":"journal-article","created":{"date-parts":[[2010,6,30]],"date-time":"2010-06-30T12:46:12Z","timestamp":1277901972000},"page":"442-451","source":"Crossref","is-referenced-by-count":291,"title":["Induction of various cytokines and development of severe mucosal inflammation by\n                    <i>cagA<\/i>\n                    gene positive\n                    <i>Helicobacter pylori<\/i>\n                    strains"],"prefix":"10.1136","volume":"41","author":[{"given":"Y","family":"Yamaoka","sequence":"first","affiliation":[{"name":"aThird Department of Internal Medicine, Kyoto Prefectural University of Medicine, 465 Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan, \n\nbDepartment of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Kita","sequence":"additional","affiliation":[{"name":"aThird Department of Internal Medicine, Kyoto Prefectural University of Medicine, 465 Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan, \n\nbDepartment of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T","family":"Kodama","sequence":"additional","affiliation":[{"name":"aThird Department of Internal Medicine, Kyoto Prefectural University of Medicine, 465 Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan, \n\nbDepartment of Microbiology, Kyoto Prefectural University of Medicine, Kyoto, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N","family":"Sawai","sequence":"additional","affiliation":[{"name":"aThird Department of Internal Medicine, Kyoto Prefectural 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