Endocrine, neural, and immune control of secretory component output by lacrimal gland acinar cells

• Published in: The Journal of immunology (1950) Vol. 146; no. 10; pp. 3405 - 3412
• Main Authors: Kelleher, RS, Hann, LE, Edwards, JA, Sullivan, DA
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-05-1991; American Association of Immunologists
• Subjects: 1-Methyl-3-isobutylxanthine - pharmacology; Animals; Biological and medical sciences; Bucladesine - pharmacology; Cells, Cultured; Cyclic AMP - physiology; Dinoprostone - pharmacology; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Hormones - pharmacology; Immunobiology; Lacrimal Apparatus - cytology; Lacrimal Apparatus - metabolism; Lymphokines - pharmacology; Male; Modulation of the immune response (stimulation, suppression); Neuropeptides - pharmacology; Rats; Rats, Inbred Strains; Secretory Component - biosynthesis; Hormone; Secretory component; IgA; Rat; Secretion; Cytokine; Rodentia; Acinus; Biosynthesis; Vertebrata; Regulation(control); Mammalia; Lacrimal gland; Mechanism of action; Neuroimmunomodulation
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.146.10.3405

Androgens regulate the synthesis and secretion of secretory component (SC), the IgA antibody receptor, by acinar cells from the lacrimal gland. However, this hormone action may be susceptible to significant modification by other agents from the endocrine, nervous, or immune systems. To investigate the nature of this neuroimmunoendocrine interaction, the present study examined the impact of hormones, neurotransmitters, and lymphokines on basal and androgen-induced SC production by lacrimal gland acinar cells in vitro. Our results demonstrated that vasoactive intestinal peptide, the beta-adrenergic agonist, isoproterenol, PGE2, IL-1 alpha, IL-1 beta, and TNF-alpha significantly increased media SC levels in control or androgen-containing cell cultures. In contrast, the cholinergic agonist, carbachol, significantly decreased cellular SC output. These effects may be mediated through the agents' known capacity to alter intracellular cAMP levels. In support of this hypothesis, exposure of acinar cells to stimulators or analogues of cAMP resulted in a significant enhancement of SC production. Thus, these findings indicate that SC output in lacrimal tissue may be modulated by interactions between the endocrine, nervous and immune systems.