Abstract
Abstract Chronic and acute stress have profound effects on inflammation. In rats, allergic inflammation is regulated by the sympathetic nervous system acting on salivary glands. Human asthma is frequently accompanied by salivary gland inflammation. Salivary gland dysfunction in stressed individuals could enhance asthma severity. Salivary gland prohormone SMR1 (submandibular rat-1) is cleaved into two peptides that are anti-inflammatory in rats, mice, dogs, sheep, cats, and human cells in pulmonary inflammation, food allergy, septic shock, pancreatitis, and spinal cord injury. We hypothesized that modulation of the autonomic nervous system would change the expression, processing, and secretion of SMR1 and its peptides. Rats were injected with saline, isoproterenol, or pilocarpine, or the superior cervical ganglion was excised. Saliva, blood, and tissues were collected and analyzed for SMR1. Adrenergic stimulation caused the majority of SMR1 into be secreted into saliva in 60 min. Removal of the superior cervical ganglion that innervates the salivary glands changed SMR1 protein levels in the salivary glands. SMR1 secretion into saliva in response to acute stress may provide a large pool of SMR1-derived peptide products that mediate anti-inflammatory responses locally and systemically. This research is funded by AllerGen NCE.
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