Abstract
The immunomodulating properties of a neuropeptide hormone, corticotropin-releasing factor (CRF), led us to investigate its effect on cAMP production by human peripheral blood mononuclear cells (MNC). In response to stimulation with CRF (100 nM), a statistically significant (P = 0.019) increase occurred in the amount of cAMP produced by MNC. Purified monocytes, but not lymphocytes, also displayed a significant (P = 0.01) increase (8- to 10-fold) in intracellular cAMP after treatment with CRF (100 nM). The antagonist α-helical CRF9-41 (100 nM) counteracted the cAMP increase induced by CRF (100 nM). The CRF-induced cAMP production was augmented by pretreatment of MNC with a cAMP-dependent protein kinase (PKA) peptide inhibitor (PI20), but was virtually unaffected by the protein kinase C (PKC) inhibitor H7, suggesting a role for cAMP signalling. Moreover, the CRF-stimulated cAMP level was reduced to baseline by intracellular Ca2+ antagonist HA1004, indicating a role for Ca2+-signalling. Based on these findings, it is concluded that cAMP and/or Ca2+ play a second messenger role in the CRF signal transduction pathway.
Original language | English |
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Pages (from-to) | 239-245 |
Number of pages | 7 |
Journal | Immunology Letters |
Volume | 35 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1993 |
Externally published | Yes |
Keywords
- cAMP
- Corticotropin-releasing factor
- Immunomodulation
- Neuroendocrine-immune axis
- Neurohormone
- Neuropeptide
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy