Eosinophil degranulation status in allergic rhinitis: observations before and during seasonal allergen exposure

Abstract

Despite the fact that extensive degranulation is a likely prerequisite for a pathogenic role of eosinophils, little is known about the degranulation status of these cells in eosinophilic conditions. The present study of the ultrastructure of tissue eosinophils explores eosinophil degranulation in allergic rhinitis before and during seasonal allergen exposure.A total of 23 patients scored symptoms q.d., prior to and during the pollen season. The numbers of mucosal eosinophils and their degranulation status were determined in nasal biopsies. Furthermore, nasal lavage fluid levels of eosinophil cationic protein (ECP) and a 2 -macroglobulin were assessed as indices of eosinophil activity and plasma exudation, respectively.Seasonal allergen exposure was associated with increased nasal symptoms, increased lavage fluid levels of ECP and a 2 -macroglobulin, and increased numbers of tissue eosinophils. In the tissue, transmission electron microscopy revealed a moderate piecemeal degranulation already prior to the season (mean¡SD 37¡2.7% altered granules). Seasonal allergen exposure increased this degranulation (87¡1.8%), and produced local areas with extensive deposition of granule proteins. The degree of eosinophil degranulation correlated with levels of ECP in lavage fluids obtained at histamine challenge.In conclusion, this study demonstrated that the nasal mucosa in allergic rhinitis features moderately degranulated eosinophils already at nonsymptomatic baseline conditions. In association with the development of symptomatic seasonal allergic rhinitis, the tissue deposition of eosinophil granule proteins is dramatically elevated through increased eosinophil numbers, together with markedly augmented degranulation of individual cells.

The Cellular Immune Response to Mycobacterium tuberculosis Infection in the Guinea Pig

“…However, because lung cell counts involve the whole digested organ the marked increase in MIL4 ϩ granulocytes in tissue homogenates seen in the chronic stage of infection likely includes these cells accumulating in airways associated with secondary lesions, as demonstrated above by immunohistochemistry. The pathogenesis of small airway inflammation in general is unclear but it may represent the transmigration of senescent inflammatory cells as a normal process of resolving inflammation (31). The significance of this process in the pathogenesis of tuberculosis may be more complicated, however, because the accumulation of granulocytes in the small airways was often observed in concert with It is unknown as yet whether the loss of T cells in the lungs and the subsequent increase in B cells and MIL4 ϩ granulocytes are related or just coincidental.…”

Mechanisms of eosinophil secretion: large vesiculotubular carriers mediate transport and release of granule-derived cytokines and other proteins

“…These gross alterations within secretory granules, indicative of progressive release of their products, are described in a diversity of cell types [7,39,40,54]. In human eosinophils, it is recognized that the number of emptying granules increases in activated cells, in vivo and in vitro, in different conditions [33][34][35][36]43]. Inflammatory stimuli, such as chemokines (eotaxin and RANTES) or platelet-activating factor, trigger PMD, and pretreatment with BFA, a potential inhibitor of vesicular transport [55], inhibits agonist-induced, granule emptying [43].…”

“…PMD is a general secretion process implicated in the release of products from activated eosinophils in a range of human diseases including allergic inflammation [33][34][35][36][37]. PMD has also been identified extensively in other secretory cells [38][39][40].…”

Correlation of Quality of Life with Clinical Parameters and Eosinophilic Cation Protein Levels in Children with Allergic Rhinoconjunctivitis

“…Eosinophil-derived mediators including eosinophilic cationic protein (ECP) damage the epithelium leading to the final clinical and pathological AR findings [1, 13, 14]. It has been reported that mucosal allergic activity is correlated with serum and local mucosal ECP levels [12]. However, the relationship between levels of inflammatory cells or markers with clinical severity is controversial [4].…”

“…AR is induced by an IgE-mediated inflammatory reaction following allergen exposure and is characterized by eosinophil infiltration and degranulation [4, 11, 12]. Eosinophil-derived mediators including eosinophilic cationic protein (ECP) damage the epithelium leading to the final clinical and pathological AR findings [1, 13, 14].…”