Medizinische Universität Graz - Research portal
Selected Publication:
Moser, A.
Immunopathology of Asthma
[ Diplomarbeit ] Medical University of Graz; 2008. pp. 82
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- Authors Med Uni Graz:
- Advisor:
- Lippe Irmgard Theresia
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- Abstract:
- Background: Allergic diseases such as atopic asthma are very common and the incidence is rising. Insights into the mechanisms of this disease bring new possibilities of intervention. Mast cell derived prostaglandin D2 may contribute to eosinophilic inflammation in allergic asthma. Chemoattractant receptor homologous molecule expressed on Th2 cells (CRTH2), mediates recruitment of Th2 cells, basophils and eosinophils to inflammatory sites. Therefore I investigated in my thesis the use of CRTH2 antagonists (CAY) in vivo in a mouse model of allergic airway inflammation. Methods: Mice were divided into four groups: OVA (ovalbumin-sensitized and challenged) mice with and without antagonist and controls. The measurement of lung function was performed after sensitization and challenge with two methods, unrestrained whole body plethysmopgraphy (WBP) and direct invasive resistance measurement with FlexiVent. Bronchoalveolar lavage and whole blood sample measurements were also performed to examine cell reactions. Results: OVA mice compared to controls showed significant elevation of eosinophils, neutrophils, lymphocytes and macrophages in the bronchoalveolar lavage (BAL) fluid. Also, OVA + CAY was significantly higher in resistance (FlexiVent) compared to controls. Eosinophils in OVA+ vehicle were significantly elevated in the whole blood sample compared to the controls. The CRTH2 antagonist showed no significant influence on cell counts in BAL or whole blood samples, but exhibited elevated resistance in the OVA + CAY group compared to controls. Measurement with whole body plethysmopgraphy showed no significant results at all. Conclusions: The results showed unclear data concerning the effect of the antagonist on airway inflammation in vivo and contrasting outcomes of measurement methods. Therefore I critically discussed the used methods, showing a reconsideration of the use of WBP. Furthermore, I contrasted chemical antagonism to a more holistic treatment of allergic diseases, using targeted infection, which induces immunoregulatory mechanisms in the host.