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dc.contributor.authorSzabo, Gyongyi
dc.contributor.authorVerma, Bikash K.
dc.contributor.authorCatalano, Donna
dc.date2022-08-11T08:09:31.000
dc.date.accessioned2022-08-23T16:34:11Z
dc.date.available2022-08-23T16:34:11Z
dc.date.issued1993-12-01
dc.date.submitted2009-03-10
dc.identifier.citation<p>J Leukoc Biol. 1993 Dec;54(6):534-44.</p>
dc.identifier.issn0741-5400 (Print)
dc.identifier.doi10.1002/jlb.54.6.534
dc.identifier.pmid7504044
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38274
dc.description.abstractEthanol consumption is associated with impaired immunity. Our data demonstrate that even a single dose of a biologically relevant concentration (25-150 mM) of ethanol can down-regulate antigen-specific T lymphocyte proliferation. In contrast, ethanol augmented mitogen-induced T cell proliferation, suggesting that its inhibitory effect on antigen-specific T cell proliferation was due to its effects on monocytes (m phi s) rather than on T cells. The immunodepressive effects of ethanol on m phi antigen-presenting cell (APC) capacity were manifested whether alcohol treatment was limited to the antigen uptake-processing period only or was present during the entire period of antigen presentation. These inhibitory effects of ethanol were also evident on both the high-antigen-presenting, Fc gamma RI-negative (-31 +/- 17%), and low-antigen-presenting, Fc gamma RI-positive (-42 +/- 15%) m phi subpopulations. Further analysis demonstrated that ethanol inhibits the production of interleukin-1 beta (IL-1 beta) and induces transforming growth factor beta (TGF-beta) and prostaglandin E2 (PGE2), monocyte-derived mediators that can affect T cell proliferation. Ethanol resulted in a dose-dependent down-regulation of secreted and cell-associated IL-1 beta protein as well as IL-1 beta mRNA levels induced by adherence or bacterial stimulation. The causal relationship between decreased m phi IL-1 beta production, elevated TGF-beta levels, and the decreased m phi APC capacity was further substantiated when exogenous IL-1 beta protein or anti-TGF-beta neutralizing antibody prevented the down-regulatory effect of ethanol on antigen-specific T cell proliferation. Utilizing a cyclooxygenase inhibitor, we also demonstrated that the ethanol-induced decrease in m phi APCs is not mediated by enhanced PGE2 production.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=7504044&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1002/jlb.54.6.534
dc.subjectAdult
dc.subjectAlcoholic Intoxication
dc.subjectAntigen-Presenting Cells
dc.subjectCell Communication
dc.subjectEpitopes
dc.subjectEthanol
dc.subjectHumans
dc.subjectLymphocyte Activation
dc.subjectMiddle Aged
dc.subjectMonocytes
dc.subjectT-Lymphocytes
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleSelective inhibition of antigen-specific T lymphocyte proliferation by acute ethanol exposure: the role of impaired monocyte antigen presentation capacity and mediator production
dc.typeArticle
dc.source.journaltitleJournal of leukocyte biology
dc.source.volume54
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1147
dc.identifier.contextkey770125
html.description.abstract<p>Ethanol consumption is associated with impaired immunity. Our data demonstrate that even a single dose of a biologically relevant concentration (25-150 mM) of ethanol can down-regulate antigen-specific T lymphocyte proliferation. In contrast, ethanol augmented mitogen-induced T cell proliferation, suggesting that its inhibitory effect on antigen-specific T cell proliferation was due to its effects on monocytes (m phi s) rather than on T cells. The immunodepressive effects of ethanol on m phi antigen-presenting cell (APC) capacity were manifested whether alcohol treatment was limited to the antigen uptake-processing period only or was present during the entire period of antigen presentation. These inhibitory effects of ethanol were also evident on both the high-antigen-presenting, Fc gamma RI-negative (-31 +/- 17%), and low-antigen-presenting, Fc gamma RI-positive (-42 +/- 15%) m phi subpopulations. Further analysis demonstrated that ethanol inhibits the production of interleukin-1 beta (IL-1 beta) and induces transforming growth factor beta (TGF-beta) and prostaglandin E2 (PGE2), monocyte-derived mediators that can affect T cell proliferation. Ethanol resulted in a dose-dependent down-regulation of secreted and cell-associated IL-1 beta protein as well as IL-1 beta mRNA levels induced by adherence or bacterial stimulation. The causal relationship between decreased m phi IL-1 beta production, elevated TGF-beta levels, and the decreased m phi APC capacity was further substantiated when exogenous IL-1 beta protein or anti-TGF-beta neutralizing antibody prevented the down-regulatory effect of ethanol on antigen-specific T cell proliferation. Utilizing a cyclooxygenase inhibitor, we also demonstrated that the ethanol-induced decrease in m phi APCs is not mediated by enhanced PGE2 production.</p>
dc.identifier.submissionpathoapubs/1147
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.contributor.departmentDepartment of Surgery
dc.source.pages534-44


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