Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-2-25
pubmed:abstractText
Although Helicobacter pylori is now recognized as playing an etiologic role in chronic gastritis and peptic ulcer disease, information on the pathogenesis and natural history of infection is limited. A model is proposed in which luminal H. pylori secrete substances that mediate inflammation that is beneficial to the organism but ultimately deleterious for the host; in addition to tissue damage, inflammation also affects gastric secretory function. In this model, the host may attempt to suppress the inflammatory response, and the adequacy of this postulated down-regulation determines pathological and clinical outcome. The effects of the inflammatory process on gastrin-hydrochloric acid homeostasis may be of critical importance in the pathogenesis of peptic ulcer disease. Because the long-term consequences of H. pylori colonization reflect the continued presence of the organism in the host over years or decades, it may be useful to consider this as a "slow" bacterial infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0016-5085
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
720-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation.
pubmed:affiliation
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review