Abstract
Introduction Eosinophils are continually targeted in allergic airway inflammatory disease therapies. The presence of their granules in airway tissues remains unexplained, yet implies the involvement of necrosis. The latter’s definition has evolved into a highly regulated and distinct signalling pathway leading to physiological inflammation, known as necroptosis. Even though necroptosis is a recently introduced concept, we currently recognize its role as an alternative mechanism in the absence of apoptosis. Furthermore, necroptosis seems to act as a host-defence strategy against viral infections, which consequently associates itself with eosinophils’ role in airway viral clearance. The aim of this review is to discuss if necroptosis of eosinophils is involved in allergic airway inflammation. Conclusion The investigation of necroptosis in eosinophil is currently an area which lacks research, yet harbours great promise for drug development.
Highlights
Eosinophils are continually targeted in allergic airway inflammatory disease therapies
Cytolysis of mucosal tissue eosinophils was induced within 1 h of an allergen challenge in guinea pigs. These findings suggest a necrotic type of eosinophil cell death rather than apoptotic, where intracellular components would remain in apoptotic bodies for proper clearance[26]
Presently, the topic of eosinophil programmed cell death (PCD) pathways is a field with many unanswered questions although it is a very promising area for drug dev elopment
Summary
Eosinophils are continually targeted in allergic airway inflammatory disease therapies. The presence of their granules in airway tissues remains unexplained, yet implies the involvement of necrosis. The aim of this review is to discuss if necroptosis of eosinophils is involved in allergic airway inflammation. Therapies triggering eosino phils, in particular corticosteroids, have greatly improved allergic and asthmatic symptoms in airways, disease management is not optimal in every case[1]. Human studies within this field continue to unveil unexplained phenomena involving eosinophils in persisting inflammation. Even though concepts discussed in this review may be applicable to other eosinophilic pathologies, this paper will be limited to the area of eosinophilic allergic airway inflammation
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