title: Role for the submandibular gland in modulating pulmonary inflammation following induction of systemic anaphylaxis.
abstract: Previous studies have shown that bilateral decentralization of the superior cervical ganglia (SCG; decentralization) attenuates allergen-induced pulmonary inflammatory responses in male rats sensitized to the nematode Nippostrongylus brasiliensis. The present report examines the neuronal and glandular mechanisms mediating the protection against pulmonary inflammation afforded by decentralization. Tissues and organs innervated by the SCG are responsible for this protection since, in a manner similar to decentralization, bilateral removal of the SCG (ganglionectomy) reduced anaphylaxis-induced accumulation of inflammatory cells in bronchoalveolar lavage fluid. Removal of the submandibular gland (sialadenectomy) did not modify the severity of the pulmonary inflammation, but concurrent sialadenectomy and decentralization abolished the protective effect of decentralization. Thus, we postulate that cervical sympathetic nerves tonically inhibit release of anti-inflammatory factors from submandibular glands. No relationship was found between noradrenaline and serotonin content of submandibular glands and the degree of protection against pulmonary inflammation offered by decentralization and ganglionectomy. Both decentralization and ganglionectomy appeared to increase the level of transcripts that encode immunomodulatory growth factors (nerve growth factor and epidermal growth factor) in submandibular glands, but these denervations evidently did not modify the transcripts for TGF beta 2. Systemic inflammatory events are regulated by the central nervous system at a level superior to the SCG probably through modulation of immunoregulatory factors in submandibular glands.
authors.affiliation: Department of Medical Physiology, Faculty of Medicine, University of Calgary, Alberta, Canada.
authors.forename: R
authors.initials: R
authors.lastname: Mathison
authors.forename: A
authors.initials: A
authors.lastname: Hogan
authors.forename: D
authors.initials: D
authors.lastname: Helmer
authors.forename: L
authors.initials: L
authors.lastname: Bauce
authors.forename: J
authors.initials: J
authors.lastname: Woolner
authors.forename: J S
authors.initials: JS
authors.lastname: Davison
authors.forename: G
authors.initials: G
authors.lastname: Schultz
authors.forename: D
authors.initials: D
authors.lastname: Befus
mesh_terms: D000707:Anaphylaxis / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000473:pathology; D002395:Catecholamines / Q000032:analysis; D004815:Epidermal Growth Factor / Q000096:biosynthesis; D005728:Ganglia, Sympathetic / Q000503:physiopathology / Q000601:surgery; D007114:Immunization; D007249:Inflammation; D008168:Lung / Q000473:pathology*; D008297:Male; D009414:Nerve Growth Factors / Q000096:biosynthesis; D009559:Nippostrongylus / Q000276:immunology; D016133:Polymerase Chain Reaction; D051381:Rats; D011919:Rats, Inbred Strains; D013363:Submandibular Gland / Q000503:physiopathology* / Q000601:surgery; D013562:Sympathectomy; D016212:Transforming Growth Factor beta / Q000096:biosynthesis
chemical_list: D002395:Catecholamines; D009414:Nerve Growth Factors; D016212:Transforming Growth Factor beta; D004815:Epidermal Growth Factor