Background: Volunteers homozygous for Glu27 beta(2)-adrenergic receptor (beta(2)AR) polymorphism have delayed onset of agonist-induced desensitization of cardiac beta(2)AR responses.
Methods And Results: To determine whether this can also be demonstrated for Glu27Glu beta(2)AR natively expressed in circulating lymphocytes, we assessed the effects of 2 weeks of oral treatment with 3 x 5 mg/d terbutaline on lymphocyte beta(2)AR density (determined by [-]-[iodine 125]iodocyanopindolol binding) and responsiveness (assessed as [-]-isoproterenol hydrochloride [INN, isoprenaline] [1 nmol/L to 1 micromol/L]-induced lymphocyte cyclic adenosine monophosphate increases) in 23 healthy volunteers (13 with wild-type beta(2)AR [group A], 5 homozygous for Glu27 with Gly16Gly or Arg16Gly [group B], and 5 homozygous for Gly16 with Gln27Gln or Gln27Glu [group C]). Before terbutaline treatment, lymphocyte beta(2)AR density and isoproterenol-induced lymphocyte cyclic adenosine monophosphate accumulation were not significantly different in the genotype groups; 2 weeks of terbutaline treatment significantly decreased lymphocyte beta(2)AR density and responsiveness in the 3 genotype groups to a nearly identical extent, and no differences were observed. In time-course studies, however, in groups A and C lymphocyte beta(2)AR showed significant (P <.05, repeated-measures ANOVA) down-regulation as early as 24 hours after the first terbutaline intake, whereas in group B significant (P <.05, repeated-measures ANOVA) beta(2)AR decreases were observed only 72 hours after the first terbutaline intake. Thus the time course of lymphocyte beta(2)AR down-regulation in group B was significantly (P <.01, 2-way ANOVA) different from that in groups A and C.
Conclusion: The extent of lymphocyte beta(2)AR down-regulation after long-term terbutaline treatment in volunteers homozygous for the Gly16 or Glu27 beta(2)AR polymorphism was genotype-independent and was nearly identical to that in wild-type beta(2)AR volunteers. However, the onset of beta(2)AR down-regulation was delayed in volunteers homozygous for the Glu27 beta(2)AR polymorphism.
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http://dx.doi.org/10.1016/S0009-9236(03)00188-7 | DOI Listing |
Pathog Dis
February 2024
Department of Applied Sciences and Mathematics, College of STEM, Bluefield State University, Bluefield, WV 24701, United States.
Chlamydia genital infection caused by Chlamydia trachomatis is the most common bacterial sexually transmitted disease worldwide. A mouse model has been developed in our laboratory to better understand the effect of cold-induced stress on chlamydia genital infection and immune response. However, the stress mechanism affecting the host response to Chlamydia muridarum genital infection remains unclear.
View Article and Find Full Text PDFFront Immunol
October 2024
Department of Biology, Concordia University, Montréal, QC, Canada.
Introduction: Adrenergic receptors regulate metabolic, cardiovascular, and immunological functions in response to the sympathetic nervous system. The effect of β-adrenergic receptor (AR) as a high expression receptor on different subpopulations of T cells is complex and varies depending on the type of ligand and context. While traditional β-AR agonists generally suppress T cells, they potentially enhance IL-17A production by Th17 cells.
View Article and Find Full Text PDFBrain Behav Immun
January 2025
School of Pharmacy, Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, Hefei, Anhui 230032, China; Institute of Clinical Immunology, Anhui Medical University, Hefei, Anhui 230032, China; Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, Anhui Medical University, Hefei, Anhui 230032, China. Electronic address:
Eur J Immunol
December 2024
Department for Immunology, Leibniz Research Centre for Working Environment and Human Factors (IfADo) at TU Dortmund, Dortmund, Germany.
Adrenergic receptors (ARs) are preferentially expressed by innate lymphocytes such as natural killer (NK) cells. Here, we study the effect of epinephrine-mediated stimulation of the β2-adrenergic receptor (β2AR) on the function of human NK cells. Epinephrine stimulation inhibited early NK cell signaling events and blocked the function of the integrin LFA-1.
View Article and Find Full Text PDFEnviron Toxicol
September 2024
School of Chemistry and Chemical Engineering, Jiangsu University, Zhenjiang, China.
Decabrominated diphenyl ether (BDE-209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE-209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear.
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