In conclusion, our findings suggest that platelet activation in the course of bacterial sepsis leads to the formation of specific PF4-bearing PMPs, which may bind to polyanionic sequences on the surface of aerobic bacteria, forming an antigenic complex that induces early formation of IgA-IgG-IgM against PF4 as part of the innate immune response. The gene discussed is PF4; the disease is bacterial infectious disease with sepsis.