Oral administration of desloratadine prior to sensitization prevents allergen-induced airway inflammation and hyper-reactivity in mice
Article first published online: 9 JUL 2004
Clinical & Experimental Allergy
Volume 34, Issue 7, pages 1124–1130, July 2004
How to Cite
Blümchen, K., Gerhold, K., Thorade, I., Seib, C., Wahn, U. and Hamelmann, E. (2004), Oral administration of desloratadine prior to sensitization prevents allergen-induced airway inflammation and hyper-reactivity in mice. Clinical & Experimental Allergy, 34: 1124–1130. doi: 10.1111/j.1365-2222.2004.01974.x
- Issue published online: 9 JUL 2004
- Article first published online: 9 JUL 2004
- Submitted 9 July 2003; revised 7 November 2003; accepted 12 March 2004
- airway inflammation;
- airway reactivity;
- Th1/Th2 cytokines
Background Histamine-1-receptor (H1R)-antagonists were shown to influence various immunological functions on different cell types and may thus be employed for immune-modulating strategies for the prevention of primary immune responses.
Objective The aim of this study was to investigate the effects of an H1R-antagonist on allergen-induced sensitization, airway inflammation (AI) and airway hyper-reactivity (AHR) in a murine model.
Methods BALB/c mice were systemically sensitized with ovalbumin (OVA) (six times, days 1–14) and challenged with aerosolized allergen (days 28–30). One day prior to the first and 2 h prior to every following sensitization, mice received either 1 or 0.01 μg of desloratadine (DL) or placebo per os.
Results Sensitization with OVA significantly increased specific and total IgE and IgG1 serum levels, as well as in vitro IL-5 and IL-4 production by spleen and peribronchial lymph node (PBLN) cells. Sensitized and challenged mice showed a marked eosinophilic infiltration in broncho-alveolar lavage fluids and lung tissues, and developed in vivo AHR to inhaled methacholine. Oral treatment with DL prior to OVA sensitization significantly decreased production of OVA-specific IgG1, as well as in vitro Th2-cytokine production by spleen and PBLN cells, compared with OVA-sensitized mice. Moreover, eosinophilic inflammation and development of in vivo AHR were significantly reduced in DL-treated mice, compared with sensitized controls.
Conclusion Treatment with H1R-anatagonist prior to and during sensitization suppressed allergen-induced Th2 responses, as well as development of eosinophilic AI and AHR. This underscores an important immune modulating function of histamine, and implies a potential role of H1R-anatagonists in preventive strategies against allergic diseases.