Browsing by Keyword "Neutrophil extracellular traps"
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Publication Hookworms Evade Host Immunity by Secreting a Deoxyribonuclease to Degrade Neutrophil Extracellular Traps.(Cell Press, 2020) Bouchery, Tiffany; Moyat, Mati; Sotillo, Javier; Silverstein, Solomon; Volpe, Beatrice; Coakley, Gillian; Tsourouktsoglou, Theodora-Dorita; Becker, Luke; Shah, Kathleen; Kulagin, Manuel; Guiet, Romain; Camberis, Mali; Schmidt, Alfonso; Seitz, Arne; Giacomin, Paul; Le Gros, Graham; Papayannopoulos, Venizelos; Loukas, Alex; Harris, Nicola L; Swiss National Science Foundation; National Health and Medical Research Council (Australia)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.Publication Neutrophils as effectors of vascular inflammation(Wiley, 2018-11) Gomez-Moreno, Diego; Adrover, Jose M; Hidalgo, Andres; Ministerio de Economía, Industria y Competitividad (España); Centro de Investigación Biomedica en Red - CIBER; Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF); Fundación ProCNICVascular inflammation underlies most forms of cardiovascular disease, which remains a prevalent cause of death among the global population. Advances in the biology of neutrophils, as well as insights into their dynamics in tissues, have revealed that these cells are prominent drivers of vascular inflammation though derailed activation within blood vessels. The development of powerful imaging techniques, as well as identification of cells and molecules that regulate their activation within vessels, including platelets and catecholamines, has been instrumental to better understand the mechanisms through which neutrophils protect or damage the organism. Other advances in our understanding of how these leucocytes exert detrimental functions on neighbouring cells, including the formation of DNA-based extracellular traps, constitute milestones in defining neutrophil-driven inflammation. Here, we review emerging mechanisms that regulate intravascular activation and effector functions of neutrophils, and discuss specific pathologies in which these processes are relevant. We argue that identification of pathways and mechanisms specifically engaged within the vasculature may provide effective therapies to treat this prevalent group of pathologies.