Infection triggered an increase in CD11b expression, adhesion to collagen, formation of mixed platelet–leucocyte aggregates, activation of NF-κB (production of IL-8 (TLR2-dependent) and IL-6) and NLRP3-derived IL-1β, neutrophil chemotaxis, and increased AXL expression. Saprophytic but not pathogenic leptospires triggered production of ROS and were phagocytized. Infection had an anti-apoptotic effect and did not activate MPO. The gene discussed is AXL; the disease is infection.