Published online: December 7, 2017
Autophagy is the cell’s housekeeping process through which dysfunctional cellular components and pathogens are cleared. Importantly, dysfunctional autophagy has been implicated in the exacerbation of diverse inflammatory diseases, including chronic rhinosinusitis (CRS). The core pathologic features of CRS include eosinophilic inflammation and elevated level of prostaglandin D2 (PGD2); however, it is not yet clear as to why these pathologic features occur in CRS.
In an article recently published in The Journal of Allergy & Clinical Immunology (JACI), Choi and colleagues utilized a murine model of CRS to provide experimental evidence that disruption of autophagy is causally linked to dysregulation of PGD2 production and eosinophilic inflammation in CRS. Also, the authors deleted the autophagy-related gene Atg7 in a cell-specific manner in order to pinpoint the role of autophagy in myeloid cells and its contribution to CRS.
The authors found that impairment of autophagy in myeloid cells led to exacerbation of CRS via aggravated eosinophilia and increased PGD2 production. They also observed that among the different types of myeloid cells, macrophages were highly affected by autophagy deficiency, and that depletion of autophagy-deficient macrophages led to significant alleviation of eosinophilic inflammation and PGD2 dysregulation.
The authors’ findings reveal the crucial role of autophagy, a basic cellular process with a pleiotropic effect on immune responses, and the importance of abnormal myeloid cells in the exacerbation of CRS and its core pathologic features. Taken together, their results imply that autophagy-enhancing drugs may be an effective therapeutic strategy for the resolution of eosinophilic inflammation in CRS.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.