The Influence of β-Adrenergic Receptor Kinase-1 on Stroke-induced Immunodeficiency Syndrome

Immunodeficiency in acute ischemic stroke (AIS) is thought to be a result of norepinephrine suppression of the lymphoid tissue. The possible differences in the distribution of lymphocytes after stroke may be due to differences in responsiveness of lymphocyte β-adrenergic receptors to their kinase (BARK-1).

The objective was to quantify the influence of lymphocyte BARK-1 on stroke-induced immunodeficiency in AIS patients.

A prospective clinical cohort study was conducted (N = 44). Measures included age, gender, race, risk factors for stroke, stroke severity, comorbidities, presence of infection, white blood cell counts and differential proportions, and lymphocyte BARK-1. Student t tests, effect sizes, and linear and logistic regressions were conducted to test the study objective. The study was approved by the Oregon Health & Science University Institutional Review Board.

There were significant changes in all white blood cells and differential proportions and in the National Institutes of Health Stroke Scale from admission to 48 hours after onset of stroke deficits. Higher BARK-1 influenced the lower lymphocyte proportion at 48 hours, independent of age, P < .0001. Furthermore, BARK-1 also was associated with an increase in the likelihood of having sustained or stroke-induced immunodeficiency at 48 hours: odds ratio, 2.41; 95% confidence interval, 1.10-5.25; P = .027, and odds ratio, 2.79; 95% confidence interval, 1.03-7.52; P = .043, respectively. In all backward stepwise selection of factors, BARK-1 was the only factor consistently retained in the models.

β-Adrenergic receptor kinase-1 has a significant quantifiable influence on lymphocyte proportion at 48 hours and on the classification of sustained stroke-induced immunodeficiency.

β-Adrenergic stimulation influences immunodeficiency in AIS.