By defining a typical infection-inflammation condition (pH 6.5 and 2 mM calcium), under which the serum kills the P. aeruginosa more effectively compared to normal physiological condition (pH 7.4 and 2.5 mM calcium), we demonstrated crosstalk between CRP and ficolin, which resulted in two new autonomous amplification pathways leading to a synergistic level of C3-deposition on the bacteria. Here, C3 is linked to infection.