Nasal eosinophilia induced by PAF-acether is accompanied by the release of eosinophil cationic protein

Abstract

N Na as sa al l e eo os si in no op ph hi il li ia a i in nd du uc ce ed d b by y P PA AF F--a ac ce et th he er r i is s a ac cc co om mp pa an ni ie ed d b by y t th he e r re el le ea as se e o of f e eo os si in no op ph hi il l c ca at ti io on ni ic c p pr ro ot te ei in n A. Tedeschi, N. Milazzo, A. Miadonna Nasal eosinophilia induced by PAF-acether is accompanied by the release of eosinophil cationic protein. A. Tedeschi, N. Milazzo, A. Miadonna. ERS Journals Ltd 1994. ABSTRACT: It has been demonstrated that platelet-activating factor (PAF)-acether can induce nasal neutrophilia and eosinophilia, with a different degree of responsiveness in atopic and in nonatopic subjects. The aim of this study was to evaluate whether PAF can also induce the release of secondary mediators in the human nose. Ten patients with allergic rhinitis and 10 normal subjects underwent nasal challenge with PAF (500 nmol), lyso-PAF (500 nmol) and saline solution. Nasal lavages were performed before and after challenge to evaluate changes in nasal cytology and release of histamine, immunoreactive leukotriene (iLT) C 4 and eosinophil cationic protein (ECP).PAF caused neutrophilia and eosinophilia, which appeared earlier in atopic than in nonatopic subjects (30 min vs 1 h), and peaked 3 h after challenge in both groups. Lyso-PAF caused mild neutrophilia, which appeared 3 h after challenge in both groups; an increase in eosinophil counts was observed 3 h after challenge in atopic subjects, but not in nonatopic subjects. PAF insufflation caused a significant release of ECP in nasal lavage fluids 30 min and 3h after challenge in atopic subjects, and 3 h after challenge in nonatopic subjects. ECP levels in the nasal lavages collected 30 min and 3 h after challenge with PAF were higher in atopic than in nonatopic subjects. Eosinophil counts correlated with ECP levels in the nasal lavages collected 30 min after PAF challenge in atopic subjects. Nasal challenge with lyso-PAF did not provoke any release of ECP. No significant increase of histamine and iLTC 4 levels in nasal lavages was found after challenge with either PAF or lyso-PAF.These results indicate that PAF-induced nasal eosinophilia is accompanied by ECP release, which appears earlier and is more marked in atopic than in nonatopic subjects.

Platelets in the immune response: Revisiting platelet-activating factor in anaphylaxis

“…[57][58][59] Biochemically, PAF challenge results in nasal hyperresponsiveness to histamine and kinins and recruitment of neutrophils and eosinophils to the nasal mucosa. 58,60,61 PAFRs are expressed in nasal mucosal epithelial cells, submucosal glands, vascular endothelial cells, mast cells, leukocytes, and lymphocytes. 62 In animal models of allergic rhinitis, PAFR antagonists reduce nasal airway resistance and vascular permeability after allergen challenge.…”

Pathophysiology of Allergic Rhinitis

“…During the immediate phase reaction, a range of chemotactic factors (cytokines, and possibly mediators such as LTB4 [36,74] and PAF [50,75] as well as neuropeptides such as substance P [76] are released by mast cells and epithelial cells and this can lead to a more complex ongoing inflammatory response. Insuf flation of PAF into the nasal cavity induces the recruitment and activation of eosinophils [77]. The recruitment of neu trophils and eosinophils by PAF is more rapid in atopic than in nonatopic subjects [78].…”

Inflammatory patterns of allergic and nonallergic rhinitis

“…Upon allergen exposure and cross-linkage of IgE, they become activated, degranulate, and release these stores [21]. Allergen activation also induces mast cell synthesis of membrane-derived mediators such as leukotrienes (LTB4, C4, D4, and E4), prostaglandins (PGD 2 ), and PAF [22] as well as bradykinin [23]. LTC4/D4 and Rhinitis is a chronic condition of the nasal mucosa that affects a large segment of the population.…”