Document Detail


Induction of peripheral lymph node addressin in human gastric mucosa infected by Helicobacter pylori.
MedLine Citation:
PMID:  15591109     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Helicobacter pylori infects over half the world's population and is a leading cause of peptic ulcer and gastric cancer. H. pylori 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 H. pylori infection is highly correlated with de novo 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.IgM 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-acetyllactosamine on extended core 1 O-glycans. These results indicate that PNAd on HEV-like vessels present in the gastric mucosa subsequent to H. pylori infection is similar to those on HEVs present in the secondary lymphoid organs, which are essential for lymphocyte circulation. Moreover, eradication of H. pylori 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 H. pylori infection.
Authors:
Motohiro Kobayashi; Junya Mitoma; Naoshi Nakamura; Tsutomu Katsuyama; Jun Nakayama; Minoru Fukuda
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-12-09
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  101     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-12-22     Completed Date:  2005-02-04     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  17807-12     Citation Subset:  IM    
Affiliation:
Glycobiology Program, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents, Non-Steroidal / adverse effects
Antigens, Surface / metabolism*
CHO Cells
Cricetinae
Gastric Mucosa / blood supply,  drug effects,  metabolism*,  microbiology*
Gastritis / chemically induced,  pathology
Helicobacter Infections / complications,  metabolism*,  microbiology,  pathology
Helicobacter pylori / physiology*
Humans
Inflammation / chemically induced,  complications,  microbiology,  pathology
Lymph Nodes / blood supply,  metabolism*,  microbiology*,  pathology
Membrane Proteins
Mice
Grant Support
ID/Acronym/Agency:
R37 CA33000/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents, Non-Steroidal; 0/Antigens, Surface; 0/L-selectin counter-receptors; 0/Membrane Proteins
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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