β2-Adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes

Mizuno, Kenji; Takahashi, Hideo; Ishibashi, Hiromi; Katsuno, Goutaro; Kamurul, Huda A.S.M.; Ohtani, Satoru; Mori, Shuji; Yoshino, Tadashi; Nishibori, Masahiro; Tanaka, Noriaki

doi:10.1016/j.imlet.2005.05.008

Cited by 35 publications

(24 citation statements)

References 27 publications

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“…These articles suggest that the β 2 -agonists are capable of inducing alterations in the Th1/Th2 cytokine balance, at least in part, via a decrease in IL-12 [24]. Additionally, Mizunoa et al [22] reported that salbutamol and terbutaline inhibit the production of LPS-induced IL-18, an IFN-γ-inducing factor, from monocytes. Moreover, fenoterol inhibits IFN-γ mRNA expression in activated PBMCs obtained from atopic asthmatics, both before and after allergen inhalation challenge [29].…”

Section: Discussionmentioning

confidence: 99%

“…Th2 cells play a crucial role in the development of airway inflammation by producing IL-4, IL-5 and IL-13, while Th1 cells produce IFN-γ. β 2 -Agonists have been reported to exert suppressive effects on Th1 cytokines [21,22]. For example, the SABA terbutaline induced a decrease in IFN-γ production in freshly isolated human monocytes stimulated by lipopolysaccharide (LPS) [22].…”

Section: Introductionmentioning

confidence: 99%

“…β 2 -Agonists have been reported to exert suppressive effects on Th1 cytokines [21,22]. For example, the SABA terbutaline induced a decrease in IFN-γ production in freshly isolated human monocytes stimulated by lipopolysaccharide (LPS) [22]. In contrast, the effects of β 2 -agonists on Th2 cytokineproduction remain controversial.…”

Section: Introductionmentioning

confidence: 99%

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Salbutamol Modulates the Balance of Th1 and Th2 Cytokines by Mononuclear Cells from Allergic Asthmatics

Yamaguchi¹,

Soma²,

Takaku³

et al. 2010

Int Arch Allergy Immunol

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Background: There is evidence that excessive use of inhalational β₂-agonists induces the deterioration of asthma. Although the exact mechanism of this remains to be elucidated, overuse of β₂-agonists may impair the Th1/Th2 balance in asthmatic airways. The aim of the present study was to evaluate whether salbutamol, a representative inhalational β₂-agonist, modifies the production of Th1- and Th2-type cytokines by mononuclear cells separated from patients with asthma and healthy volunteers. Methods: Peripheral blood mononuclear cells (PBMCs) obtained from 8 healthy volunteers and 10 patients with mild persistent asthma allergic to house dust mites were treated with either salbutamol or medium alone. PBMCs were then stimulated with either medium alone, house dust mite (Dermatophagoides farina, Df) allergen or a combination of ionomycin plus phorbol 12-myristate 13-acetate ester (PMA). Concentrations of IFN-γ, IL-13, TNF-α and RANTES in the cell supernatants were measured using ELISA. Results: In PBMCs from healthy volunteers, salbutamol did not modify IFN-γ production, but increased the spontaneous production of IL-13. In contrast, salbutamol significantly inhibited the spontaneous and ionomycin- plus PMA-stimulated production of IFN-γ by PBMCs from asthmatics. Salbutamol significantly enhanced both spontaneous and Df-induced production of IL-13 by PBMCs from asthmatics. Salbutamol did not modify the production of TNF-α. Finally, salbutamol enhanced the production of RANTES induced by Df allergen in asthmatics. Conclusions: Salbutamol inhibits IFN-γ and enhances IL-13 production by PBMCs from asthmatics. These effects would promote a Th1/Th2 imbalance in the airways and may therefore contribute to the deterioration of asthma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Salbutamol Modulates the Balance of Th1 and Th2 Cytokines by Mononuclear Cells from Allergic Asthmatics

Yamaguchi¹,

Soma²,

Takaku³

et al. 2010

Int Arch Allergy Immunol

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“…No significant evidence supports a direct association between the B2AR and NO synthases; however, there are several possible indirect links that have been suggested. First, NO synthases may be transcriptionally regulated in response to cytokines [36,37], and cytokines may be regulated or inhibited by B2AR [38,39]. Secondly, NO, as a messenger molecule, is related to endothelial mechanisms of vasodilation due to the stimulation of the B2AR [40].…”

Section: Discussionmentioning

confidence: 99%

β₂-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking

Wilson

Bush²

2007

Eur Respir J

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The aim of the present study was to assess the effects of possible interactions between b 2 -adrenoceptor gene polymorphisms and passive smoking on forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and exhaled nitric oxide (eNO) in children aged 11 yrs.A cross-sectional analysis of the longitudinal cohort was conducted for associations between b 2 -adrenoceptor gene polymorphisms and lung function and eNO with regard to passive smoking.Among children exposed to tobacco smoke, those with Arg16 (at least one Arg allele) exhibited lower adjusted mean FEV1 (2.19 versus 2.38 L) and FVC (2.43 versus 2.64 L) than Gly16 homozygotes. Those with Gln27 (at least one Gln allele) also exhibited a lower adjusted mean FEV1 relative to Glu27 homozygotes (2.24 versus 2.39 L). Among children with no exposure to smoking, those with Arg16 or Gln27 showed lower adjusted geometric mean eNO levels compared with Gly16 homozygotes (15.4 versus 30.9 ppb) and Glu27 homozygotes (18.0 versus 49.7 ppb).In conclusion, passive smoking had a significant effect on associations between b 2 -adrenoceptor gene polymorphisms and asthma-related phenotypes, enhancing the relationship between Arg16 and lung function and removing the relationship between Arg16 or Gln27 and exhaled nitric oxide levels.

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“…Additionally, the stress-induced increase in ␤AR receptor expression in the liver, specifically ␤1AR signaling on F4/80 ϩ cells, implicates catecholamine-induced changes in monocytes. It is known that catecholamines alter macrophage redox state (40 -42) and early inflammatory cytokine profiles (43)(44)(45).…”

Section: Discussionmentioning

confidence: 99%

β1-Adrenergic Receptors on Immune Cells Impair Innate Defenses against Listeria

Emeny

Gao

Lawrence

2007

The Journal of Immunology

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Cold restraint (CR) for 1 h elicits a psychological and physiological stress that inhibits host defenses against Listeria monocytogenes (LM). Previous analyses indicated that this inhibition is not due to depletion of B or T cells but is instead dependent on signaling through β-adrenoceptors (βARs). We now show that impaired host resistance by CR cannot be accounted for by a decrease in LM-specific (listeriolysin O91–99 tetramer+) effector CD8+ T cells; this result is consistent with previous observations that CR-induced effects are mainly limited to early anti-LM responses. β2-Adrenoceptor (β2AR)−/− FVB/NJ and wild-type FVB/NJ mice had equivalent anti-LM defenses, whereas β1-adrenoceptor (β1AR)−/− FVB/NJ mice had lower levels of LM even when subjected to CR treatment. Additionally, host-resistance competency of β1AR−/− mice could be transferred to irradiated wild-type mice reconstituted with β1AR−/− bone marrow progenitors and spleen cells, indicating that β1AR signaling on immune cells reduces anti-LM responses. β1AR−/− mice had improved cellular (delayed-type hypersensitivity) responses while β2AR−/− mice had improved humoral responses (IgG1, IgG2, and IgM), a result that further explains the strain differences in LM defenses. CR-induced expression of β1AR and β2AR mRNA was assessed by real-time PCR. CR treatment significantly increased βAR mRNAs in Ficoll-purified and F4/80+-enhanced liver but not splenic homogenates, demonstrating an organ-specific effect of stress that alters host defenses. Finally, CR treatment induced early increases in perforin expression that may enhance immune cell apoptosis and interfere with LM clearance. In conclusion, β1AR signaling has immunomodulatory effects on early cell-mediated immune responses; a lack of β1AR signaling improves antilisterial defenses and cell-mediated immunity, in general.

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β2-Adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes

Cited by 35 publications

References 27 publications

Salbutamol Modulates the Balance of Th1 and Th2 Cytokines by Mononuclear Cells from Allergic Asthmatics

Salbutamol Modulates the Balance of Th1 and Th2 Cytokines by Mononuclear Cells from Allergic Asthmatics

β₂-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking

β1-Adrenergic Receptors on Immune Cells Impair Innate Defenses against Listeria

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β2-Adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes

Cited by 35 publications

References 27 publications

Salbutamol Modulates the Balance of Th1 and Th2 Cytokines by Mononuclear Cells from Allergic Asthmatics

Salbutamol Modulates the Balance of Th1 and Th2 Cytokines by Mononuclear Cells from Allergic Asthmatics

β2-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking

β1-Adrenergic Receptors on Immune Cells Impair Innate Defenses against Listeria

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β₂-Adrenoceptor polymorphisms and asthma phenotypes: interactions with passive smoking