Linked Life Data

8123217

Source:http://linkedlifedata.com/resource/pubmed/id/8123217

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-4-14
pubmed:abstractText
Alcoholics have frequent bronchial and intestinal bacterial-associated infections compromising the mucosal-associated lymphoid tissues. Alcoholics also suffer undernutrition due to changes in their lifestyles. Thus, we studied the intestinal mucosa-associated lymphoid tissues using two types of diets in young and mature mice. The objective was to elucidate if ethanol consumption alters the T and B cell populations in the intestine, and if the alteration could be associated with the age and/or the nutritional status of the host. There was an increase in the number of CD8+ cells per field in the intestinal lamina propria (ILP) of young mice consuming ethanol, with no change in CD4+ and IgA+ cells in the ILP and CD4+ and CD8+ cells in the intestinal intraepithelium (IE). There was also an increase in the number of CD4+ and CD8+ cells in the ILP of well-nourished mature mice consuming ethanol, and an increase in the number of CD4+ cells in the ILP of undernourished mice. An increase in the number of CD8+ cells in the IE was also detected in the well-nourished group consuming ethanol. Therefore, we conclude that ethanol administration alters the intestinal mucosa-associated lymphoid tissue.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0741-8329
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
555-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Ethanol-induced changes in the intestinal mucosa-associated immune system of young and mature mice.
pubmed:affiliation
Department of Family and Community Medicine, University of Arizona, Tucson 85724.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.