UC San Diego

Objective

To synthesize investigations into the role of lipid-mediated recruitment and activation of group 2 innate lymphoid cells (ILC2s) in aspirin-exacerbated respiratory disease (AERD).

Data sources

A comprehensive literature review of reports pertaining to cellular mechanisms, cytokine, and lipid mediators in AERD, as well as ILC2 activation and recruitment, was performed using PubMed and Google Scholar.

Study selections

Selections of studies were based on reports of lipid mediators in AERD, cytokine mediators in AERD, type 2 effector cells in AERD, platelets in AERD, AERD treatment, ILC2s in allergic airway disease, and ILC2 activation, inhibition, and trafficking.

Results

The precise mechanisms of AERD pathogenesis are not well understood. Greater levels of proinflammatory lipid mediators and type 2 cytokines are found in tissues derived from patients with AERD relative to controls. After pathognomonic cyclooxygenase-1 inhibitor reactions, proinflammatory mediator concentrations (prostaglandin D2 and cysteinyl leukotrienes) are rapidly increased, as are ILC2 levels in the nasal mucosa. The ILC2s, which potently generate type 2 cytokines in response to lipid mediator stimulation, may play a key role in AERD pathogenesis.

Conclusion

Although the literature suggests that lipid-mediated ILC2 activation may occur in AERD, there is a dearth of definitive evidence. Future investigations leveraging novel next-generation single-cell sequencing approaches along with recently developed AERD murine models will better define lipid mediator-induced ILC2 trafficking in patients with AERD.