Chronic stress exposure is hypothesized to increase the risk for developing a mental or physical disease, which can be summarized as an overall increased vulnerability to adverse health conditions. This thesis shows one potential pathway of stress exposure entering the body via activation of the hypothalamus pituitary adrenal (HPA) axis and the interaction between HPA axis and immune activation. Chronic stress caused by work overload or the experience of stressful life events was associated with altered levels of cortisol, the main effector hormone of the HPA axis. Further, chronic stress was shown to effect the distribution of neutrophils, a leukocyte subtype known for its defence properties as well as for its side effects of tissue damage. Additional analyses support a theory that HPA axis and immune cells work in synergy to adapt the organism to chronic stress exposure and therefore represent one pathway how stress can cause altered immune defence toward an increased vulnerability to disease.
| Identifer | oai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:75830 |
| Date | 01 September 2021 |
| Creators | Penz, Marlene Sophie |
| Contributors | Kirschbaum, Clemens, Rohleder, Nicolas, Technische Universität Dresden |
| Source Sets | Hochschulschriftenserver (HSSS) der SLUB Dresden |
| Language | English |
| Detected Language | English |
| Type | info:eu-repo/semantics/acceptedVersion, doc-type:doctoralThesis, info:eu-repo/semantics/doctoralThesis, doc-type:Text |
| Rights | info:eu-repo/semantics/openAccess |
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