Introduction: IL−13 is a Th2 cytokine that has a potential pivotal role in allergic and asthmatic responses, including airway remodelling. Our objective was to evaluate the effects of anti−IL−13 on the inflammatory response following repetitive NAC in seasonal allergic rhinitis. Study design: A parallel group double−blind placebo−controlled study (n=16 and 15) with an open label group given topical nasal corticosteroids (n=5). Subjects received intranasal Timothy grass pollen (Phleum P5 allergen), and serial samples were taken using Synthetic Absorptive Matrix (Accuwik Ultra) and by nasal lavage. NAC was performed at screening and on days 5, 6 and 7 following infusion of anti−IL−13 or placebo. Results: Anti−IL−13 was found to profoundly inhibit levels of IL−13, and to a lesser extent eotaxin in SAM eluates during the late phase after NAC. However, there were no apparent effects on levels of nasal lavage eosinophils nor nasal symptom scores. In contrast, topical nasal corticosteroid caused pronounced suppression of IL−13, IL−5 and eotaxin in the late phase, inhibited the levels of lavage eosinophils, and decreased symptom scores in the late phase. Conclusions: Anti−IL−13 has specific pharmacodynamic target action, causing profound inhibition of nasal IL−13 responses. However, failure to inhibit nasal symptoms and eosinophils, suggests anti−IL−13 is not critical to the acute nasal allergic response. Further studies are now required to assess the effects of anti−IL−13 in asthma; and especially to elucidate effects on the airways in terms of inflammation, hyperreactivity and remodelling. This abstract is funded by: Novartis Pharmaceuticals.

No abstract