Highlight : Eosinophil extra - cellular traps in Allergy

Eosinophil degranulation has always aroused the interests of physicians and scientists alike. Loss of viability and release of membrane-free granules upon eosinophil degranulation was first demonstrated by Gleich and coworkers in 1996. These free eosinophil granules, once considered as crush artifacts, are now confirmed products of eosinophil cytolysis, and suggested to be significantly pathogenic. In 2013, Weller and group described eosinophil degranulation associated with cell death, eosinophil-derived extra-cellular traps (EETs) and release of free granules; an event termed as EETosis. This form of degranulation is mechanistically different to the earlier described mitochondrial DNA traps released by live eosinophils by Simon and co-workers (2008); the presence of which were next demonstrated in biopsy tissues from eosinophilic skin disorders (2011). This “highlighted” study by Ueki et al. (2016) describes for the first time the presence of EETs in tissue samples obtained from patients with eosinophilic chronic rhinosinusitis, thereby providing a clinical significance to this event of eosinophil cytolysis with nuclear EETs. When contacted, Dr. Paige Lacy (University of Alberta, co-author of the chapter “Signaling and Degranulation” in Eosinophils in Health and Disease), commented that this paper “evaluated the ability of EETs to entrap microorganisms such as S. aureus, E. coli, and C. albicans by means of passive contact, and showed that eosinophil-derived DNA was capable of ensnaring these microorganisms in a similar manner to neutrophil NETs. Interestingly, eosinophil-derived DNA promoted binding through non-electrostatic hydrophobic interactions, rather than what might be more intuitively considered through hydrophilic association. Finally, EETs were shown to be more stable structures than NETs because of reduced intrinsic protease activity that eosinophils possess relative to neutrophils.” In summary, this study sheds light on a novel mechanism of mediator release from eosinophils that may have important clinical implications for patients with eosinophilic diseases.