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The β1-Adrenergic Receptor Contributes to Sepsis-Induced Immunosuppression Through Modulation of Regulatory T-Cell Inhibitory Function*

Manon Durand, Eugénie Hagimont, Huguette Louis, Pierre Asfar, Jean‐Pol Frippiat, Mervyn Singer, Guillaume Gauchotte, Carlos Labat, Patrick Lacolley, Bruno Lévy, Benjamin G. Chousterman, Antoine Kimmoun

2022UCL Discovery (University College London)23 citations

Abstract

OBJECTIVES: Although cardiovascular benefits of β1-adrenergic receptor blockade have been described in sepsis, little is known about its impact on the adaptive immune response, specifically CD4 T cells. Herein, we study the effects of β1-adrenergic receptor modulation on CD4 T-cell function in a murine model of sepsis. DESIGN: Experimental study. SETTING: University laboratory. SUBJECTS: C57BL/6 mice. INTERVENTIONS: High-grade sepsis was induced by cecal ligation and puncture in wild-type mice (β1+/+) with or without esmolol (a selective β1-adrenergic receptor blocker) or in β1-adrenergic receptor knockout mice (β1-/-). At 18 hours after surgery, echocardiography was performed with blood and spleen collected to analyze lymphocyte function. MEASUREMENTS AND MAIN RESULTS: At 18 hours, β1+/+cecal ligation and puncture mice exhibited characteristics of high-grade sepsis and three surrogate markers of immunosuppression, namely decreased splenic CD4 T cells, reduced CD4 T-cell proliferation, and increased regulatory T lymphocyte cell proportions. Pharmacologic and genetic β1-adrenergic receptor blockade reversed the impact of sepsis on CD4 T and regulatory T lymphocyte proportions and maintained CD4 T-cell proliferative capacity. β1-adrenergic receptor blocked cecal ligation and puncture mice also exhibited a global decrease in both pro- A nd anti-inflammatory mediators and improved in vivo cardiovascular efficiency with maintained cardiac power index despite the expected decrease in heart rate. CONCLUSIONS: β1-adrenergic receptor activation enhances regulatory T lymphocyte inhibitory function and thus contributes to sepsis-induced immunosuppression. This can be attenuated by β1-adrenergic receptor blockade, suggesting a potential immunoregulatory role for this therapy in the management of sepsis.

Topics & Concepts

MedicineImmunosuppressionInhibitory postsynaptic potentialSepsisFunction (biology)AdrenergicReceptorCell biologyAdrenergic receptorPharmacologyImmunologyInternal medicineBiologyIntensive Care Unit Cognitive DisordersThermal Regulation in MedicineCancer, Stress, Anesthesia, and Immune Response
The β1-Adrenergic Receptor Contributes to Sepsis-Induced Immunosuppression Through Modulation of Regulatory T-Cell Inhibitory Function* | Litcius