ArticleJournal of innate immunity2014
Induction of M2 regulatory macrophages through the β2-adrenergic receptor with protection during endotoxemia and acute lung injury.
Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed.
- Neuroinflammation and noradrenergic modulation with β2-adrenoceptors: Emerging therapeutic targets for Parkinson's diseases.Neural regeneration research · 2026Article
- The Role of the Nervous System in Lung Disease.Current neurology and neuroscience reports · 2026Review
- Neural modulation of ocular immunity: Exploring a sympathetic-macrophage neuroimmune link in the human ciliary body.Journal of anatomy · 2026Article
- The active role of pulmonary immunity in ischaemic stroke.Journal of neuroinflammation · 2026Review
- Rats exposed to a low resource environment in early life display sex differences in blood pressure, autonomic activity, and brain and kidney pro-inflammatory markers during adulthood.Biology of sex differences · 2026Article
- Prognostic significance of beta-adrenergic receptor expression in oesophageal adenocarcinoma.The journal of pathology. Clinical research · 2026Article
- Targeting the Neuro-Immune Axis in Next-Generation Oncology: Discovery and Validation of βOncology research · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities.Frontiers in physiology · 2026Review
- The hallmarks of neuro-immune reprogramming in cancer.Frontiers in immunology · 2026Review
- The crosstalk between nerves and immunity: chronic stress as a driver of tumor progression.Frontiers in immunology · 2026Review
- Adrenergic receptors: a key determinant of outcomes in bacterial pneumonia and bacterial sepsis-associated acute lung injury/acute respiratory distress syndrome through participation in pulmonary innate immune response.Frontiers in immunology · 2026Review
- Non-selective beta-blockers enhance resolution of induced infections in animals and healthcare-associated infections in humans.Scientific reports · 2025Article
- Sympathetic regulation of the host immune response to bacterial sepsis.Clinical science (London, England : 1979) · 2025Review
- Exosomes and MicroRNAs: key modulators of macrophage polarization in sepsis pathophysiology.European journal of medical research · 2025Review
- The effects of ultra-selective beta1-antagonism on the metabolic and cytokine profile in septic shock patients receiving noradrenaline: a sub-investigation from the STRESS-L Randomised Study.Intensive care medicine experimental · 2025Article
- Adrenergic signaling during parasitic infections.Frontiers in immunology · 2025Review
- Formoterol Reduces the Pro-Inflammatory Phenotype by Enhancing the Activity of Glutaminase in Monocyte-Derived Macrophages in the CVB3-Induced Viral Myocarditis.Immunity, inflammation and disease · 2024Article
- Review
- Peripheral and central regulation of neuro-immune crosstalk.Inflammation and regeneration · 2024Review
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The main drivers of acute inflammation are macrophages, which are known to have receptors for catecholamines. Based on their function, macrophages are broadly categorized as having either M1 (proinflammatory) or M2 phenotypes (anti-inflammatory). In this study, we investigated catecholamine-induced alterations in the phenotype of activated macrophages. In the presence of lipopolysaccharide (LPS), mouse peritoneal macrophages acquired an M1 phenotype. However, the copresence of LPS and either epinephrine or norepinephrine resulted in a strong M2 phenotype including high levels of arginase-1 and interleukin-10, and a reduced expression of M1 markers. Furthermore, epinephrine enhanced macrophage phagocytosis and promoted type 2 T-cell responses in vitro, which are known features of M2 macrophages. Analysis of M2 subtype-specific markers indicated that LPS and catecholamine-cotreated macrophages were not alternatively activated but were rather of the regulatory macrophage subtype. Interestingly, catecholamines signaled through the β2-adrenergic receptor but not the canonical cAMP/protein kinase A signaling pathway. Instead, the M2 pathway required an intact phosphoinositol 3-kinase pathway. Blockade of the β2-adrenergic receptor reduced survival and enhanced injury in mouse models of endotoxemia and LPS-induced acute lung injury, respectively. These results demonstrate a role for the β2-adrenergic receptor in promoting the M2 macrophage phenotype.
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