Release of secretory immunoglobulin A by submandibular gland via β adrenergic receptor stimulation

•β receptor stimulation increased secretory IgA release from submandibular gland.•sIgA secretion by isoprenaline stimulation was dose dependent.•Inhibition of β receptor by propranolol blocked sIgA secretion. Secretory immunoglobulin A (sIgA) is important for mucosal immunity due to the inhibition of pathogen infection. The submandibular gland is known to secrete more sIgA than the parotid and sublingual glands. In this study, we focused on the relationship between the secretion of accumulated intracellular sIgA and β-adrenergic receptor stimulation, and clarified the autonomic regulatory mechanism of sIgA secretion in submandibular gland cells using dispersed gland cells. Sprague-Dawley rats (male, 6 weeks old, 200–250 g) were euthanized and their submandibular glands were removed. Dispersed submandibular gland cells placed in Krebs-Ringer-Bicarbonate solution were stimulated by autonomic nerve agonists. The concentration of secreted sIgA was measured using a rat IgA ELISA kit. The results were analysed using ANOVA and Tukey’s test. Cells stimulated with the non-selective β-adrenoreceptor agonist, isoprenaline, secreted significantly more sIgA compared with the unstimulated control. The β2-adrenoreceptor agonist, fenoterol, caused significantly more sIgA secretion than the control, and more sIgA secretion than the β1-adrenoreceptor agonist, xamoterol. sIgA secretion by isoprenaline stimulation was dose dependent. Inhibition of the β receptor by propranolol completely blocked sIgA secretion following isoprenaline stimulation. Stimulation of β receptors could result in more secretion of intracellularly accumulated sIgA compared with stimulation of other autonomic receptors in the autonomic modulation of mucosal immunity.