{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T10:25:12Z","timestamp":1791109512109,"version":"4.1.0"},"reference-count":40,"publisher":"National Academy of Sciences","issue":"51","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2004,12,21]]},"abstract":"<jats:p>\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    infects over half the world's population and is a leading cause of peptic ulcer and gastric cancer.\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection results in chronic inflammation of the gastric mucosa, and progression of chronic inflammation leads to glandular atrophy and intestinal metaplasia. However, how this chronic inflammation is induced or maintained is not well known. Here, we show that chronic inflammation caused by\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection is highly correlated with\n                    <jats:italic>de novo<\/jats:italic>\n                    synthesis of peripheral lymph node addressin (PNAd) presented on high-endothelial venule (HEV)-like vessels. The number of HEV-like vessels dramatically increases as chronic inflammation progresses. We found that the PNAd is bound by L-selectin\u00b7IgM chimeric protein, and decorated by NCC-ST-439 antibody, which is suggested to recognize both nonsulfated and 6-sulfated sialyl Lewis X on core 2 branched O-glycans, and MECA-79 antibody, which reacts with 6-sulfo\n                    <jats:italic>N<\/jats:italic>\n                    -acetyllactosamine on extended core 1 O-glycans. These results indicate that PNAd on HEV-like vessels present in the gastric mucosa subsequent to\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection is similar to those on HEVs present in the secondary lymphoid organs, which are essential for lymphocyte circulation. Moreover, eradication of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    is associated with the disappearance of HEV-like vessels in the gastric mucosa. By contrast, very few PNAd were found in the gastric mucosa of patients with chemical gastritis caused by nonsteroidal antiinflammatory drugs. These results strongly suggest that PNAd in HEV-like vessels plays a critical role in lymphocyte recruitment during chronic inflammation induced by\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0407503101","type":"journal-article","created":{"date-parts":[[2004,12,9]],"date-time":"2004-12-09T20:14:30Z","timestamp":1102623270000},"page":"17807-17812","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":104,"title":["Induction of peripheral lymph node addressin in human gastric mucosa infected by\n                    <i>Helicobacter pylori<\/i>"],"prefix":"10.1073","volume":"101","author":[{"given":"Motohiro","family":"Kobayashi","sequence":"first","affiliation":[{"name":"Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; and Departments of Pathology, Internal Medicine, and Laboratory Medicine, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junya","family":"Mitoma","sequence":"additional","affiliation":[{"name":"Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; and Departments of Pathology, Internal Medicine, and Laboratory Medicine, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naoshi","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; and Departments of Pathology, Internal Medicine, and Laboratory Medicine, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tsutomu","family":"Katsuyama","sequence":"additional","affiliation":[{"name":"Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; and Departments of Pathology, Internal Medicine, and Laboratory Medicine, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Nakayama","sequence":"additional","affiliation":[{"name":"Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; and Departments of Pathology, Internal Medicine, and Laboratory Medicine, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minoru","family":"Fukuda","sequence":"additional","affiliation":[{"name":"Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037; and Departments of Pathology, Internal Medicine, and Laboratory Medicine, Shinshu University School of Medicine, Matsumoto 390-8621, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2004,12,9]]},"reference":[{"key":"e_1_3_2_1_2","first-page":"1311","year":"1984","unstructured":"Marshall, B. 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