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• W2238861146 endingPage "L682" @default.
• W2238861146 startingPage "L675" @default.
• W2238861146 abstract "In addition to their well-studied bronchodilatory and cardiotonic effects, beta-adrenergic agonists carry anti-inflammatory properties by inhibiting cytokine production by human mononuclear cells. In a model of human promonocytic THP-1 cells stimulated with lipopolysaccharide (LPS), we showed that beta-agonists inhibited tumor necrosis factor-alpha and interleukin-8 production predominantly via the beta(2)-adrenergic receptor through the generation of cAMP and activation of protein kinase A. This effect was reproduced by other cAMP-elevating agents such as prostaglandins and cAMP analogs. Activation and nuclear translocation of the transcription factor nuclear factor-kappaB induced by LPS were inhibited with treatment with beta-agonists, an effect that was prominent at late time points (>1 h). Although the initial IkappaB-alpha degradation induced by LPS was minimally affected by beta-agonists, the latter induced a marked rebound of the cytosolic IkappaB-alpha levels at later time points (>1 h), accompanied by an increased IkappaB-alpha cytoplasmic half-life. This potentially accounts for the observed nuclear factor-kappaB sequestration in the cytoplasmic compartment. We postulate that the anti-inflammatory effects of beta-agonists reside in their capacity to increase cytoplasmic concentrations of IkappaB-alpha, possibly by decreasing its degradation." @default.
• W2238861146 created "2016-06-24" @default.
• W2238861146 creator A5034641437 @default.
• W2238861146 creator A5056099545 @default.
• W2238861146 date "2000-10-01" @default.
• W2238861146 modified "2023-10-17" @default.
• W2238861146 title "β-Adrenergic agonists exert their “anti-inflammatory” effects in monocytic cells through the IκB/NF-κB pathway" @default.
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• W2238861146 doi "https://doi.org/10.1152/ajplung.2000.279.4.l675" @default.
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