Utilizza questo identificativo per citare o creare un link a questo documento: http://elea.unisa.it/xmlui/handle/10556/4475
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dc.contributor.authorPiazza, Ornella
dc.contributor.authorStaiano, Rosaria I.
dc.contributor.authorDe Robertis, Edoardo
dc.contributor.authorConti, Guido
dc.contributor.authorDi Crescenzo, Vincenzo
dc.contributor.authorLoffredo, Stefania
dc.contributor.authorMarone, Giancarlo
dc.contributor.authorZito Marinosci, Geremia
dc.contributor.authorCataldi, Mauro
dc.date.accessioned2020-05-22T12:01:39Z
dc.date.available2020-05-22T12:01:39Z
dc.date.issued2016
dc.identifier.citationPiazza O, Staiano RI, De Robertis E, Conti G, Di Crescenzo V, Loffredo S, Marone G, Zito Marinosci G, Cataldi M. Effect of α2-adrenergic agonists and antagonists on cytokine release from human lung macrophages cultured in vitro. Translational Medicine @ UniSa 2016, 15(9): 67-73.it_IT
dc.identifier.issn2239-9747it_IT
dc.identifier.urihttp://www.translationalmedicine.unisa.it/indexit_IT
dc.identifier.urihttp://elea.unisa.it:8080/xmlui/handle/10556/4475
dc.identifier.urihttp://dx.doi.org/10.14273/unisa-2673-
dc.description.abstractThe most trusted hypothesis to explain how α2-adrenergic agonists may preserve pulmonary functions in critically ill patients is that they directly act on macrophages by interfering with an autocrine/paracrine adrenergic system that controls cytokine release through locally synthetized noradrenaline and α1- and α2-adrenoreceptors. We tested this hypothesis in primary cultures of resident macrophages from human lung (HLMs). HLMs were isolated by centrifugation on percoll gradients from macroscopically healthy human lung tissue obtained from four different patients at the time of lung resection for cancer. HLMs from these patients showed a significant expression of α2A, α2B and α2C adrenoreceptors both at the mRNA and at the protein level. To evaluate whether α2 adrenoreceptors controlled cytokine release from HMLs, we measured IL-6, IL-8 and TNF-α concentrations in the culture medium in basal conditions and after preincubation with several α2- adrenergic agonists or antagonists. Neither the pretreatment with the α2-adrenergic agonists clonidine, medetomidine or dexdemetomidine or with the α2-adrenergic antagonist yohimbine caused significant changes in the response of any of these cytokines to LPS. These results show that, different from what reported in rodents, clonidine and dexdemetomidine do not directly suppress cytokine release from human pulmonary macrophages. This suggests that alternative mechanisms such as effects on immune cells activation or the modulation of autonomic neurotransmission could be responsible for the beneficial effects of these drugs on lung function in critical patients.it_IT
dc.format.extentP. 67-73it_IT
dc.language.isoenit_IT
dc.sourceUniSa. Sistema Bibliotecario di Ateneoit_IT
dc.subjectClonidineit_IT
dc.subjectDexmedetomidineit_IT
dc.subjectMedetomidineit_IT
dc.subjectYohimbineit_IT
dc.subjectCytokinesit_IT
dc.subjectMacrophagesit_IT
dc.titleEffect of α2-adrenergic agonists and antagonists on cytokine release from human lung macrophages cultured in vitroit_IT
dc.typeArticleit_IT
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