title: Diminished proliferation of B blast cell in response to cytokines in ethanol-consuming mice.
abstract: We and others have demonstrated that ethanol suppresses the antibody response in humans and animals. The purpose of this study was to determine whether ethanol affects cytokine-induced proliferative responses of splenic B blast cells, and whether the decreased response was due to an imbalance of the cytokine activity. Thus, the ability of spleen cells from individual ethanol-diet-fed C57BL/6 mice to proliferate and produce cytokines was determined. The ability of anti-IgM monoclonal antibodies (mAb)-activated splenic B blast cells in response to mouse recombinant IL-2 (rIL-2) or rIL-4 was also assessed. A thymidine incorporation assay was used to determine cell proliferation, and the conventional bioassays for cytokine-dependent cell proliferation were used for determining the bioactivity of cytokines. Data were analyzed with general linear model procedure. Our results showed that ethanol weakened the proliferative response of B cells in response to mitogen as well as to mouse rIL-2 and rIL-4. The decreased B cell responses may result from an increase in the production of IL-4 by helper T cells. Finally, in the presence of excessive dose of rIL-4, the proliferative responses of B blast cells from all three groups of mice were diminished (p<0.01). Thus, our data clearly indicated that the diminished B cell proliferation in ethanol-consuming mice was due in part to an excessive amount of IL-4 produced and an inability of the B cell to interact properly with IL-4 that was secreted by helper T cells. The results should extend our basic understanding of the mechanism by which chronic alcoholism impairs the interactions and interdependence of T- and B-cell immune functions.
authors.affiliation: Geriatric Research, Education and Clinical Center, VA Medical Center, West Los Angeles, CA 90073, USA.
authors.forename: Mei-Ping
authors.initials: MP
authors.lastname: Chang
authors.forename: Qun
authors.initials: Q
authors.lastname: Wang
authors.forename: Dean C
authors.initials: DC
authors.lastname: Norman
mesh_terms: D000437:Alcoholism / Q000276:immunology; D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000911:Antibodies, Monoclonal / Q000276:immunology; D001402:B-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D002455:Cell Division / Q000187:drug effects / Q000276:immunology; D000431:Ethanol / Q000633:toxicity*; D007376:Interleukin-2 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000378:metabolism / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011994:Recombinant Proteins / Q000494:pharmacology*; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D007376:Interleukin-2; D011994:Recombinant Proteins; C044203:anti-IgM; D015847:Interleukin-4; D000431:Ethanol