Immunoendokrinologie bei Stress – Interaktion von Cortisol und Makrophagen Migrationsinhibierendem Faktor (MIF) bei akutem und chronischem Stress im Menschen
Bei akutem und chronischem Stress kommt es zu einer Reihe physiologischer Reaktionen im Körper. Die wohl wichtigste Rolle auf neuroendokriner Ebene spielt die Hypothalamus-Hypophysen-Nebennierenrinden-Achse (HHNA), deren Aktivierung zu einer vermehrten Freisetzung von Cortisol führt. Auch das Imm...
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Format: | Doctoral Thesis |
Language: | German |
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Philipps-Universität Marburg
2009
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Online Access: | PDF Full Text |
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Acute and chronic stress results in an activation of the hypothalamic-pituitary-adrenal axis (HPA-axis), which induces an increased cortisol-release. Also the immune system reacts on stress, especially by transfer of cytokines like IL-6 and TNF- Macrophage migration inhibitory factor (MIF) was discovered as one of the first cytokines in the early sixties. MIF acts on one side as a counterregulator of the anti-inflammatory and immunosuppressive activities of glucocorticoids, on the other side induce low concentrations of glucocorticoids themselves the MIF-secretion. Furthermore MIF was found in the anterior lobe of the pituitary gland where it is partly located in secretory granules together with adrenocorticotrop hormone (ACTH). Corticotropin releasing hormone (CRH) was found to be a potent secretagogue that causes the release of MIF from corticotrophic cells at lower concentrations than necessary for ACTH-release. To study the relation between the cortisol and MIF in acute stress we examined MIF and cortisol in the saliva of healthy young people in a physiological stress-paradigm. In depressive patients it’s described a condition of chronic stress. Serum- and salivary-MIF and cortisol has been measured in these patients in the course of disease and compared to healthy controls. After acute stress the salivary cortisol-levels showed a significant increase, the MIF-levels showed no significant reaction. Looking at the people with a high cortisol-reaction and those who showed no cortisol-reaction after acute stress a difference in the course of MIF-levels could not be found. Dividing the group after basal MIF-levels, people with continuous low salivary MIF-levels showed a significant higher cortisol-reaction after stress, whereas people with high MIF-concentrations showed a significant weaker cortisol-reaction. This was particularly found in men where also a negative correlation could be seen. The depressive patients showed no significant higher cortisol-levels in saliva and serum in comparison to the healthy controls and there was no difference in MIF-levels between these groups. Also in depressive patients in the course differences in cortisol- and MIF-levels in saliva and serum could not be found. Though, it could be noticed a significant negative correlation between cortisol and MIF in the serum, people with high MIF-levels showed low cortisol-concentrations and vice versa. Concerning the interaction of MIF and cortisol one could conclude as follows: There is a negative correlation between basal MIF- and cortisol-levels in the serum. This correlation could not be found in the saliva. High salivary MIF-levels inhibit the cortisol-increase after acute stress. This was not studied in serum.