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Hookworms Evade Host Immunity by Secreting a Deoxyribonuclease to Degrade Neutrophil Extracellular Traps. 2020
Tiffany Bouchery, and
Mati Moyat, and
Javier Sotillo, and
Solomon Silverstein, and
Beatrice Volpe, and
Gillian Coakley, and
Theodora-Dorita Tsourouktsoglou, and
Luke Becker, and
Kathleen Shah, and
Manuel Kulagin, and
Romain Guiet, and
Mali Camberis, and
Alfonso Schmidt, and
Arne Seitz, and
Paul Giacomin, and
Graham Le Gros, and
Venizelos Papayannopoulos, and
Alex Loukas, and
Nicola L Harris
Laboratory of Intestinal Immunology, Department of Immunology and Pathology, Monash University, Melbourne, VIC 3004, Australia; Laboratory of Intestinal Immunology, SV, Ecole Polytechnique Federale de Lausanne (EPFL), Lausanne CH-1015 Switzerland.
Hookworms cause a major neglected tropical disease, occurring after larvae penetrate the host skin. Neutrophils are phagocytes that kill large pathogens by releasing neutrophil extracellular traps (NETs), but whether they target hookworms during skin infection is unknown. Using a murine hookworm, Nippostrongylus brasiliensis, we observed neutrophils being rapidly recruited and deploying NETs around skin-penetrating larvae. Neutrophils depletion or NET inhibition altered larvae behavior and enhanced the number of adult worms following murine infection. Nevertheless, larvae were able to mitigate the effect of NETs by secreting a deoxyribonuclease (Nb-DNase II) to degrade the DNA backbone. Critically, neutrophils were able to kill larvae in vitro, which was enhanced by neutralizing Nb-DNase II. Homologs of Nb-DNase II are present in other nematodes, including the human hookworm, Necator americanus, which also evaded NETs in vitro. These findings highlight the importance of neutrophils in hookworm infection and a potential conserved mechanism of immune evasion.
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