title: Secretion of IgA by rat parotid and submandibular cells in response to autonomimetic stimulation in vitro.
abstract: The major antibody in saliva is IgA, which is actively transported by pIgR expressed by parenchymal cells within the salivary glands. The rate of IgA secretion into saliva is regulated by the autonomic nerves supplying the glands in vivo. This study examined the mechanism of increased IgA secretion into saliva with autonomimetic stimulation. In vitro stimulation of IgA secretion from cells prepared by digestion of rat salivary glands found submandibular cell preparations responded to alpha- and beta-adrenergic stimuli whereas the parotid cells responded only to beta-adrenergic stimulation, although cells from both glands responded similarly to cholinergic stimulation. The additional responsiveness of submandibular cells to alpha-adrenergic stimulation probably reflects the presence of granular duct cells (absent in parotid glands) which are known to secrete protein in response to high frequency sympathetic stimulation. The increased secretion of IgA was not dependant upon increased plasma cell activation since isolated salivary gland plasma cells did not respond to agonists. Further evidence for the regulating role of parenchymal cells in IgA secretion into saliva was revealed by analysis of polymeric immunoglobulin receptor (pIgR) levels expressed on cells. Following in vivo nerve stimulation, there was an increased amount of pIgR expressed on the membrane surface. This was functionally demonstrated in vitro by increased uptake of human IgA by acutely prepared rat salivary cells following stimulation by adrenaline, indicating increased mobilisation of pIgR with stimulation. This study confirms that salivary cells increase the delivery of IgA into saliva by a pIgR-mediated mechanism in response to autonomic stimulation.
authors.affiliation: Salivary Research Group, Guy's King's and St. Thomas' School of Dentistry, The Rayne Institute, 123 Coldharbour Lane, London SE5 9NU, UK. guy.carpenter@kcl.ac.uk
authors.forename: Guy H
authors.initials: GH
authors.lastname: Carpenter
authors.forename: Gordon B
authors.initials: GB
authors.lastname: Proctor
authors.forename: Lorna E
authors.initials: LE
authors.lastname: Ebersole
authors.forename: John R
authors.initials: JR
authors.lastname: Garrett
mesh_terms: D000318:Adrenergic beta-Agonists / Q000008:administration & dosage / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D002217:Carbachol / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D004837:Epinephrine / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D007070:Immunoglobulin A / Q000378:metabolism*; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D015213:Neuroimmunomodulation; D010306:Parotid Gland / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010656:Phenylephrine / Q000008:administration & dosage / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D019056:Receptors, Polymeric Immunoglobulin / Q000096:biosynthesis; D013363:Submandibular Gland / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D007070:Immunoglobulin A; D019056:Receptors, Polymeric Immunoglobulin; D010656:Phenylephrine; D002217:Carbachol; D011433:Propranolol; D007545:Isoproterenol; D004837:Epinephrine