Evaluation of the anti-inflammatory effects of β-adrenoceptor agonists on human lung macrophages

Gill, Sharonjit K; Marriott, Helen M.; Suvarna, S K; Peachell, Peter T.

doi:10.1016/j.ejphar.2016.11.005

Cited by 10 publications

(10 citation statements)

References 32 publications

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“…In this study, we evidenced similar effect of catecholamines and b2agonist on porcine BMM, as previously demonstrated on porcine alveolar and liver macrophages (Izeboud et al, 2000). Our data using b2-agonist are also in agreement with data obtained on human macrophages, except for IL-8 that was found unchanged by Donnelly et al (Donnelly et al, 2010;Gill et al, 2016). Concordantly, we recently reported an impaired secretion of IL-8 and TNFa by porcine LPS-stimulated leukocytes in whole blood assay following acute stress that we attributed to catecholamine burst (Bacou et al, 2017).…”

Section: Discussionsupporting

confidence: 92%

β2-adrenoreceptor stimulation dampens the LPS-induced M1 polarization in pig macrophages

Bacou

Haurogné

Allard

et al. 2017

Developmental & Comparative Immunology

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The cross-talk between sympatho-adreno-medullar axis and innate immunity players was mainly studied in rodents. In intensive husbandry, pigs are exposed to multiple stressors inducing repeated releases of catecholamines that bind to adrenoreceptors (AR) on target cells. Among adrenoreceptors, the β2-AR is largely expressed by immune cells including macrophages. We report herein on the effects of catecholamines, through β2-AR stimulation, on pig macrophage functions activated by LPS. β2-AR stimulation of porcine macrophages prevented the LPS-induced increase in TNFα and IL-8 secretion while increasing IL-10 secretion. In contrast, treatment with a β2-agonist had no effect on anti-microbial functions. Lastly, β2-AR stimulation of macrophages reduced the expression of genes up-regulated by LPS. Altogether, we demonstrated that β2-AR stimulation of porcine macrophages prevented polarization towards a pro-inflammatory phenotype. Since porcine macrophages are a suitable model for human macrophages, our results might be relevant to appreciate catecholamine effects on human macrophages.

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Section: Discussionsupporting

confidence: 92%

β2-adrenoreceptor stimulation dampens the LPS-induced M1 polarization in pig macrophages

Bacou

Haurogné

Allard

et al. 2017

Developmental & Comparative Immunology

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“…Similarly, bronchodialator indacaterol, which targets the exonuclease is also a promising agent due to its ability to regulate genes involved in suppressing pro-inflammatory cytokine production and attenuation of immune response [139] , [140] , [141] . Another study has reported indacaterol to be able to bind spike protein of SARS-CoV2 [142] .…”

Section: Discussionmentioning

confidence: 99%

Identification of multipotent drugs for COVID-19 therapeutics with the evaluation of their SARS-CoV2 inhibitory activity

Kumar

Singh

Kumari

et al. 2021

Computational and Structural Biotechnology Journal

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“…Both in vitro and in vivo studies support the conclusion that at least one way in which β-adrenergic signaling can promote breast cancer progression is by polarizing macrophages toward an M2 phenotype ( 42 , 43 ). Moreover, in response to LPS stimulation, human monocyte-derived macrophages produce reduced amounts of the inflammatory cytokines TNF-α, IL-1β, CCL2, CCL3, and CCL4 ( 47 – 49 ) and decrease IL-27 secretion in response to acute inflammation ( 50 ) while, at the same time, increasing production of the anti-inflammatory cytokines IL-4, IL-10, and IL-13 production ( 44 , 50 ). In contrast to the effects of β-AR signaling in macrophage, α-AR signaling promotes secretion of pro-inflammatory cytokines ( 24 , 51 ).…”

Section: Neural Regulation Of the Immune Responsementioning

confidence: 99%

Adrenergic Signaling: A Targetable Checkpoint Limiting Development of the Antitumor Immune Response

et al. 2018

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An immune response must be tightly controlled so that it will be commensurate with the level of response needed to protect the organism without damaging normal tissue. The roles of cytokines and chemokines in orchestrating these processes are well known, but although stress has long been thought to also affect immune responses, the underlying mechanisms were not as well understood. Recently, the role of nerves and, specifically, the sympathetic nervous system, in regulating immune responses is being revealed. Generally, an acute stress response is beneficial but chronic stress is detrimental because it suppresses the activities of effector immune cells while increasing the activities of immunosuppressive cells. In this review, we first discuss the underlying biology of adrenergic signaling in cells of both the innate and adaptive immune system. We then focus on the effects of chronic adrenergic stress in promoting tumor growth, giving examples of effects on tumor cells and immune cells, explaining the methods commonly used to induce stress in preclinical mouse models. We highlight how this relates to our observations that mandated housing conditions impose baseline chronic stress on mouse models, which is sufficient to cause chronic immunosuppression. This problem is not commonly recognized, but it has been shown to impact conclusions of several studies of mouse physiology and mouse models of disease. Moreover, the fact that preclinical mouse models are chronically immunosuppressed has critical ramifications for analysis of any experiments with an immune component. Our group has found that reducing adrenergic stress by housing mice at thermoneutrality or treating mice housed at cooler temperatures with β-blockers reverses immunosuppression and significantly improves responses to checkpoint inhibitor immunotherapy. These observations are clinically relevant because there are numerous retrospective epidemiological studies concluding that cancer patients who were taking β-blockers have better outcomes. Clinical trials testing whether β-blockers can be repurposed to improve the efficacy of traditional and immunotherapies in patients are on the horizon.

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Evaluation of the anti-inflammatory effects of β-adrenoceptor agonists on human lung macrophages

Cited by 10 publications

References 32 publications

β2-adrenoreceptor stimulation dampens the LPS-induced M1 polarization in pig macrophages

β2-adrenoreceptor stimulation dampens the LPS-induced M1 polarization in pig macrophages

Identification of multipotent drugs for COVID-19 therapeutics with the evaluation of their SARS-CoV2 inhibitory activity

Adrenergic Signaling: A Targetable Checkpoint Limiting Development of the Antitumor Immune Response

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