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      Pituitary Adenylate-Cyclase-Activating Polypeptide Expression in the Immune System

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          Although pituitary adenylate-cyclase-activating polypeptide (PACAP) is a multifunctional and pleiotropic neuropeptide with many different immunomodulatory properties, investigations of its source in lymphoid organs are scarce. The present report contributes to the knowledge on the origin and synthesis of this peptide in immune cells of the lymphoid organs and peritoneum using immunohistochemistry, immunocytochemical staining, Western blot and RT-PCR methods. Our study reveals PACAP immunoreactivity in the thymus, spleen and lymph nodes. Cytochemical results show that PACAP is present in thymocytes, lymphocytes and plasma cells from the spleen and lymph nodes. Western blot analysis showed a band corresponding to PACAP for all lymphoid organs studied. mRNA appears in both double (CD4+CD8+)- and single-positive (CD4+CD8–, CD4–CD8+) thymocytes and in T subsets and B cells from the spleen and lymph nodes. In addition, PACAP mRNA is expressed in lymphocytes, but not in macrophages from peritoneal suspensions. Our findings show that PACAP produced by lymphocytes could be added to the growing list of mediators shared by nervous, endocrine and immune systems. Moreover, PACAP could be considered as a lymphocyte-derived cytokine in the central and peripheral lymphoid organs acting on lymphocytes and stromal cells.

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          Most cited references 11

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          Vasoactive intestinal peptide prevents experimental arthritis by downregulating both autoimmune and inflammatory components of the disease.

          Rheumatoid arthritis (RA) is a chronic and debilitating autoimmune disease of unknown etiology, characterized by chronic inflammation in the joints and subsequent destruction of the cartilage and bone. We describe here a new strategy for the treatment of arthritis: administration of the neuropeptide vasoactive intestinal peptide (VIP). Treatment with VIP significantly reduced incidence and severity of arthritis in an experimental model, completely abrogating joint swelling and destruction of cartilage and bone. The therapeutic effect of VIP was associated with downregulation of both inflammatory and autoimmune components of the disease. Our data indicate VIP as a viable candidate for the development of treatments for RA.
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            Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibit tumor necrosis factor alpha transcriptional activation by regulating nuclear factor-kB and cAMP response element-binding protein/c-Jun.

            Tumor necrosis factor alpha (TNFalpha), an early cytokine produced by activated macrophages, plays an essential role in normal and pathological inflammatory reactions. The excessive production of TNFalpha is prevented by the so-called "macrophage-deactivating factors." This study examines the role of two structurally related neuropeptides, the vasoactive intestinal peptide (VIP) and the pituitary adenylate cyclase-activating peptide (PACAP), as inhibitors of TNFalpha. Both VIP and PACAP inhibit TNFalpha production from lipopolysaccharide-stimulated RAW 246.7 cells in a dose- and time-dependent manner. Although the activated cells express mRNA for all three VIP/PACAP receptors, agonist and antagonist studies indicate that the major receptor involved is VIP1R. VIP/PACAP inhibit TNFalpha gene expression by affecting both NF-kB binding and the composition of the cAMP responsive element binding complex (CREB/c-Jun). Two transduction pathways, a cAMP-dependent and a cAMP-independent pathway, are involved in the inhibition of TNFalpha gene expression and appear to differentially regulate the transcriptional factors involved. Because TNFalpha plays a central role in various inflammatory diseases such as endotoxic shock, multiple sclerosis, cerebral malaria, and various autoimmune conditions, the down-regulatory effect of VIP/PACAP may have a significant therapeutic potential.
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              Human Peripheral Blood Mononuclear Cells Express Gonadotropin-Releasing Hormone (GnRH), GnRH Receptor, and Interleukin-2 Receptor  -Chain Messenger Ribonucleic Acids That Are Regulated by GnRH in Vitro

               H.-F. Chen (1999)

                Author and article information

                S. Karger AG
                December 2002
                19 December 2002
                : 10
                : 3
                : 177-186
                Department of Cellular Biology, Faculty of Biology, Complutense University, Madrid, Spain
                67180 Neuroimmunomodulation 2002–03;10:177–186
                © 2002 S. Karger AG, Basel

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                Figures: 4, References: 47, Pages: 10
                Original Paper


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