Sarcoptes scabiei Induces Discrete NET Release, Ca2+ Fluxes and ROS Production Without Impairing Phagocytic Activity in Bovine Polymorphonuclear Neutrophils.

Sarcoptic mange is a skin disease caused by Sarcoptes scabiei infestations, characterized by dermatitis, pruritus, and exudative responses in both humans and animals. Biologically, the life cycle of S. scabiei is confined to the host's skin (stratum corneum), where mite-derived molecules trigger the influx of innate immune cells, including polymorphonuclear neutrophils (PMN), which play a central role in skin inflammatory responses. The antimicrobial activity of PMNs is regulated by Ca2+ fluxes and includes the generation of reactive oxygen species (ROS), degranulation, and the release of neutrophil extracellular traps (NETs). NETs are web-like structures composed of chromatin and enzymes that can trap and eventually kill pathogens; however, their involvement in S. scabiei infestations in bovines remains unclear. Here, we investigated interactions between bovine PMN and S. scabiei mites, as well as PMN responses to S. scabiei antigen (ScAg). Functional parameters included NET release, Ca2+ fluxes, ROS production and phagocytic activity, determined by fluorescence microscopy, Fluo-4 staining, luminol-derived luminescence and flow cytometry, respectively. Current data show that ScAg, but not whole mites, induces a weak NET release in exposed bovine PMN. Additionally, ScAg drives rapid and sustained Ca2+ fluxes and ROS production over time, without altering the phagocytic capacity of PMN.