Factors contributing to nasal allergic late phase eosinophilia

The diagnosis and management of rhinitis: An updated practice parameter

“…LTC 4 increases both during the early-phase and late-phase nasal responses to allergen. 716 In a study evaluating kinetics of mediators and cytokines in nasal secretions after allergen challenge, histamine was increased in nasal secretions during the early-phase and late-phase nasal responses, and IL-1b and IL-4 were significantly elevated during the late-phase response. 712 In another study that examined nasal mucosal late responses after a single nasal grass allergen exposure, T H 2 cytokines including IL-5 and IL-13 were expressed in association with increased numbers of eosinophils.…”

Nasal inflammatory mediators and specific IgE production after nasal challenge with grass pollen in local allergic rhinitis

“…These results reflect eosinophil activation during the immediate and late response to nasal challenge in patients with LAR, not just during the late response, as has been reported in atopic patients. 27,[29][30][31] An important finding of this study was the detection of significantly increased nasal levels of sIgE to grass pollen at 1, 6, and 24 hours after NAPT in 30% of the patients with LAR. This rapid nasal release of sIgE after nasal challenge, with the detection in some patients of baseline levels of sIgE to grass pollen out of spring, supports the existence of a persistent local synthesis of sIgE in nasal mucosa of patients with LAR that rapidly enhances after nasal exposure to aeroallergens.…”

“…It has been used in previous studies as a specific marker for eosinophil activation in late responses to NAPT in subjects with allergic rhinitis, showing a significant increase 4 to 9 hours after challenge. 29,30 In our group of patients with LAR, the release of ECP was detected 15 minutes after the NAPT, and then increased progressively, reaching the maximum nasal concentration at 24 hours after provocation. There were no differences between an immediate and a dual response.…”

Fluticasone Furoate Inhibits Cytokine Secretion from Nasal Epithelial Cells and Reduces Eosinophil Survival in an in vitro Model of Eosinophilic Inflammation

“…In fact, in nasal secretions from patients suffering from AR, increased concentrations have been reported in eotaxin [1], granulocyte-macrophage colony-stimulating factor (GM-CSF) [2,3], interleukin (IL)-1β [2,4], IL-5 [2,5,6,7,8], IL-6 [2,3], IL-8 [1,3,4], IL-13 [8] and RANTES [9] as well as other mediators such as adhesion molecules [5], tryptase [6,7] and eosinophil cationic protein (ECP) [6]. In addition, the presence of eosinophils in both nasal secretions and nasal mucosa (NM) are also characteristic of AR [10,11].…”