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dc.contributor.authorVerma, Bikash K.
dc.contributor.authorFogarasi, Miklos C.
dc.contributor.authorSzabo, Gyongyi
dc.date2022-08-11T08:08:37.000
dc.date.accessioned2022-08-23T16:01:18Z
dc.date.available2022-08-23T16:01:18Z
dc.date.issued1993-01-01
dc.date.submitted2010-04-21
dc.identifier.citationJ Clin Immunol. 1993 Jan;13(1):8-22.
dc.identifier.issn0271-9142 (Linking)
dc.identifier.pmid8445046
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31088
dc.description.abstractAs the most commonly used drug that can modulate both metabolic and immune pathways, ethanol is evaluated in this report as a regulator of tumor necrosis factor alpha (TNF alpha) production in human peripheral blood monocytes (M phi) in combination with a variety of stimuli. While acute ethanol treatment did not induce TNF alpha in M phi, it was a potent down-regulator of M phi TNF alpha production whether induced by the combination of interferon-gamma plus muramyl dipeptide (MDP) (P < 0.001), lipopolysaccharide (LPS) alone (P < 0.01), or interferon-gamma plus LPS. Down-regulation of M phi TNF alpha by ethanol was dose dependent and statistically significant in the biologically relevant, 25-150 mM, ethanol concentration range. We also demonstrate that these ethanol concentrations did not affect M phi viability. TNF alpha down-regulation by ethanol was most effective when ethanol was administered 4 hr prior to MDP stimulation; however, it was also effective--though to a lesser extent--if it was added at the time of MDP stimulation. Furthermore, ethanol also down-regulated TNF alpha production of the in vivo preactivated M phi of trauma patients, which produce hyperelevated levels of TNF alpha. We have previously shown that the majority of posttrauma elevated M phi TNF alpha is produced by the M phi subpopulation expressing high-affinity type I Fc gamma receptors (Fc gamma RI). When the Fc gamma RI cross-linking-stimulated M phi subpopulation was treated with acute ethanol, TNF alpha production was suppressed again both in in vivo preactivated M phi of trauma patients and in M phi of normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8445046&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1007/BF00920631
dc.subjectAcetylmuramyl-Alanyl-Isoglutamine
dc.subjectAdult
dc.subjectAged
dc.subjectCell Adhesion
dc.subjectCell Separation
dc.subjectCell Survival
dc.subjectDinoprostone
dc.subjectDose-Response Relationship, Drug
dc.subjectDown-Regulation
dc.subjectEthanol
dc.subjectFemale
dc.subjectFlow Cytometry
dc.subjectHumans
dc.subjectIndomethacin
dc.subjectInterferon-gamma
dc.subjectMacrophage Activation
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectMonocytes
dc.subjectReceptors, IgG
dc.subjectTumor Necrosis Factor-alpha
dc.subjectDigestive System Diseases
dc.subjectGastroenterology
dc.titleDown-regulation of tumor necrosis factor alpha activity by acute ethanol treatment in human peripheral blood monocytes
dc.typeJournal Article
dc.source.journaltitleJournal of clinical immunology
dc.source.volume13
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gastroenterology_pp/15
dc.identifier.contextkey1282308
html.description.abstract<p>As the most commonly used drug that can modulate both metabolic and immune pathways, ethanol is evaluated in this report as a regulator of tumor necrosis factor alpha (TNF alpha) production in human peripheral blood monocytes (M phi) in combination with a variety of stimuli. While acute ethanol treatment did not induce TNF alpha in M phi, it was a potent down-regulator of M phi TNF alpha production whether induced by the combination of interferon-gamma plus muramyl dipeptide (MDP) (P < 0.001), lipopolysaccharide (LPS) alone (P < 0.01), or interferon-gamma plus LPS. Down-regulation of M phi TNF alpha by ethanol was dose dependent and statistically significant in the biologically relevant, 25-150 mM, ethanol concentration range. We also demonstrate that these ethanol concentrations did not affect M phi viability. TNF alpha down-regulation by ethanol was most effective when ethanol was administered 4 hr prior to MDP stimulation; however, it was also effective--though to a lesser extent--if it was added at the time of MDP stimulation. Furthermore, ethanol also down-regulated TNF alpha production of the in vivo preactivated M phi of trauma patients, which produce hyperelevated levels of TNF alpha. We have previously shown that the majority of posttrauma elevated M phi TNF alpha is produced by the M phi subpopulation expressing high-affinity type I Fc gamma receptors (Fc gamma RI). When the Fc gamma RI cross-linking-stimulated M phi subpopulation was treated with acute ethanol, TNF alpha production was suppressed again both in in vivo preactivated M phi of trauma patients and in M phi of normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)</p>
dc.identifier.submissionpathgastroenterology_pp/15
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.contributor.departmentDepartment of Surgery
dc.source.pages8-22


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