Table 2 The effect of the eosinophil extracellular traps (EETs) on other types of cells

Airway epithelial cell

A549, BEAS-2B, human primary small airway epithelial cells and mouse model

EETs caused dose-dependent changes in the morphology and density of A549 cells, leading to more than 10% cell detachment and increased epithelial permeability. Moreover, EETs significantly increased the release of epithelium-derived cytokines, inducing a type 2 immune response

[11, 93]

PNECs

PAD4 ^−/− mouse model and H146 cells

EET induces PNEC to secrete neuropeptides and neurotransmitters, exacerbating asthma inflammation.

[10]

ILC2s

EETs-stimulated mouse model l

Altered activation status of ILC2 in lung tissue of EET-treated mice and increased proportion of IL-5 or IL-13 producing ILC2 in the lung.

[11]

Eosinophils

Purified eosinophils isolated from human peripheral blood

Consistent with PMA stimulation, the induction of EETs led to morphological changes in eosinophils and significantly increased eosinophil degranulation and ROS production. However, both effects were found to be weaker compared to the effects of PMA stimulation.

[93]

Macrophages

primary human monocyte-derived macrophages differentiated from CD14 + monocytes

CLCs, a component of EETs, can release the pro-inflammatory cytokine IL-1β upon induction of phagocytosis by primary human macrophages in vitro

[22]