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A toll-like receptor 2/6-agonist prevents allergic airway inflammation in chronic respiratory sensitisation

: Fuchs, B.; Knothe, S.; Rochlitzer, S.; Matthias, N.; Greweling, M.; Lauenstein, H.; Nassenstein, C.; Müller, M.; Ebensen, T.; Krug, N.; Dittrich, A.; Guzman, C.; Braun, A.

Allergy. European journal of allergy and clinical immunology 63 (2008), Supplement s88, pp.407
ISSN: 0105-4538
ISSN: 1398-9995
European Academy of Allergology and Clinical Immunology (EAACI Congress) <27, 2008, Barcelona>
Fraunhofer ITEM ()

Background: The hygiene hypothesis negatively correlates the microbial burden of the environment to the prevalence of Th2-related disorders, e.g. allergy and asthma. This is explained by a Th1-triggering through pathogen-associated patterns sensed via toll-like receptors.
Objective: To discover mechanisms which prevent the development of chronic allergic inflammation.
Methods: In a chronic model of allergic airway inflammation induced by intranasal Timothy grass pollen allergen extract administrations, early-onset toll-like receptor agonisation and/or interferon-a˜ administration was compared to the therapeutic and immune-modulating effects of dexamethasone.
Results: By toll-like receptor 2/6-agonisation allergic inflammation and airway remodelling were reduced. Lymphocyte counts were not changed, nor did the cytokine profile or the number of CD41foxp31cells in draining lymph nodes prove a Th2/Th1-shift or the induction of tolerance. Dexamethasone reduced both sensitisation as well as allergic inflammation, and, moreover, CD11c1cells in lymph nodes. Stimulation experiments point to a general unresponsiveness of splenocytes after toll-like receptor agonisation, implicating a T-cell anergy.
Conclusion: The toll-like receptor 2/6-agonist is a promising preventive approach in diseases related to exaggerated T-cell responses, e.g., allergy, and asthma.