Eosinophils from Physiology to Disease: A Comprehensive Review

Figure 3

United airways disease. Local inflammatory events at the level of the nasal mucosa and paranasal sinuses can correlate with ongoing inflammation in the lungs. Inherited and environmental factors cooperate in the development of such pathological scenario. Eosinophil-dominant responses play a central role in this setting and become active following several stimuli. Conventional allergic responses might prompt mast cell-assisted or direct eosinophil activation, when nasal or paranasal residing cells are challenged with aerial allergens and recognise systemically produced IgE. However, local production of IgE may also occur. Adaptive immune responses can be stimulated by the persistence of inflammatory triggers or by forced superantigenic activation in the setting of Staphylococcus aureus colonisation of the mucosal tissues. Disproportionate production of mucosal secretion and loss of tissue integrity due to persistent inflammation may paradoxically favour microbial proliferation and promote further inflammation. A mixture of infectious and allergic features characterises Aspergillus colonisation of the paranasal sinuses. Anti-Aspergillus IgE account for enhanced eosinophil inflammation. Mast cells are involved in a crucial cross-talk with eosinophils and may dominate the pathogenic cascade in selected conditions such as nonallergic rhinitis with mast cells (NARMA) or eosinophil-mast cell nonallergic rhinitis (NARESMA). Eicosanoids play a major role in this setting as they have vasomotor effects and promote eosinophil recruitment and activation. Nonsteroidal anti-inflammatory drugs may affect this signalling pathway and cause non-IgE-related hypersensitivity reactions at the level of both the upper and lower respiratory tract. In particular, the so-called aspirin exacerbated respiratory disease (AERD) is characterised by a constitutional overproduction of CysLTs, which can be further enhanced by COX-1 inhibitors such acetylsalicylic acid (ASA).