Microfilariae Trigger Eosinophil Extracellular DNA Traps in a Dectin-1-Dependent Manner

Eosinophils mediate protection against filarial nematodes. Our results demonstrate that eosinophil extracellular traps (EETosis) are induced by microfilariae and infective L3 larvae of Litomosoides sigmodontis. These extracellular DNA traps inhibit microfilariae motility in a DNA- and contact-dependent manner in vitro. Accordingly, microfilariae-injection triggers DNA release in an eosinophil-dependent manner in vivo and microfilariae covered with DNA traps are cleared more rapidly. Using dectin-1, we identify the required receptor for the microfilariae-induced EETosis, whereas signaling via other C-type lectin receptors, prior priming of eosinophils, and presence of antibodies are not required. The DNA released upon microfilariae-induced EETosis is mainly of mitochondrial origin, but acetylated and citrullinated histones are found within the traps. We further demonstrate that the presented DNA-dependent inhibition of microfilariae motility by eosinophils represents a conserved mechanism, as microfilariae from L. sigmodontis and the canine heartworm Dirofilaria immitis induce ETosis in murine and human eosinophils. [Display omitted] •Eosinophils release extracellular DNA traps and inhibit microfilariae motility•Microfilariae-induced eosinophil extracellular DNA traps are a conserved mechanism•Microfilariae trigger DNA release by eosinophils through the dectin-1 receptor•Microfilariae coated with DNA traps are cleared more efficiently in vivo Parasitic filariae (thread worms) cause debilitating diseases, and eosinophils are essential for protective immune responses against filariae. The mechanism by which eosinophils mediate protection is not fully understood. Ehrens et al. emphasize the importance of eosinophil extracellular DNA traps in trapping infective larval stages and the progeny of filarial worms.