Document Detail


Mechanism of the impaired T-cell proliferation in adult rats exposed to alcohol in utero.
MedLine Citation:
PMID:  8045674     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although attempts have been made to assess the effect of ethanol on the immune responses in individuals with fetal alcohol syndrome, there is no consensus as to the effect of ethanol on the immune system. Evidence that fetal alcohol-exposed (FAE) humans and animals have diminished proliferative response of T-cells to mitogenic lectins is well established. However, little is known about the mechanism of a toxic effect of ethanol on T-cell growth. Thus, a rat model was used to delineate the mode of ethanol action on T-cell proliferation. We found that the diminished T-cell proliferation in young adult FAE rats was due to a decreased responsiveness to interleukin 2 (IL2), but not to an impaired production of IL2 and expression of IL2 receptors (IL2R). Furthermore, the decreased proliferative response did not result from the presence of an excessive suppressor T-cell activity. Measurements of [Ca+2]i and T-cell proliferation were concurrently performed in batches of cells from the same animals. It was demonstrated that an increase in [Ca+2]i induced by Concanavalin A (Con A) in T-cells from FAE rats was not impaired, although the T-cell proliferation induced by Con A was significantly diminished. The results of the IL2-binding study showed that the Kd values and the number of both high- and low-affinity IL2R binding sites on the T-cells of FAE rats were comparable to those of pair-, or chow-fed rats. Finally, the results of the kinetics and rate of the internalization of IL2 showed that (1) the amount of the internalized IL2 was significantly reduced in T-cells from FAE rats, and (2) the half-time (t1/2) for dissociation of IL2 from the receptors in the T-cells from FAE rats was also greater than that of the control rats. These results taken together indicate that ethanol suppresses T-cell proliferation by interfering with events following the IL2-IL2R interaction.
Authors:
M P Chang; D T Yamaguchi; M Yeh; A N Taylor; D C Norman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  International journal of immunopharmacology     Volume:  16     ISSN:  0192-0561     ISO Abbreviation:  Int. J. Immunopharmacol.     Publication Date:  1994 Apr 
Date Detail:
Created Date:  1994-09-01     Completed Date:  1994-09-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7904799     Medline TA:  Int J Immunopharmacol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  345-57     Citation Subset:  IM    
Affiliation:
Education and Clinic Center (GRECC), Veteran Administration Medical Center, West Los Angeles, CA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Surface / immunology
Calcium / metabolism
Cell Cycle
Cell Division / drug effects
Concanavalin A / pharmacology
Ethanol / toxicity*
Female
Fetal Alcohol Syndrome / immunology*
Flow Cytometry
Interleukin-2 / biosynthesis
Pregnancy
Rats
Rats, Sprague-Dawley
Receptors, Interleukin-2 / biosynthesis,  drug effects
Spleen / cytology,  drug effects
T-Lymphocytes / drug effects*,  metabolism
Chemical
Reg. No./Substance:
0/Antigens, Surface; 0/Interleukin-2; 0/Receptors, Interleukin-2; 11028-71-0/Concanavalin A; 64-17-5/Ethanol; 7440-70-2/Calcium

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


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