Virulent "P. gingivalis" further modulates leukocyte recruitment by proteolysis of cytokines and chemokines that are secreted by the host cells. The arg-gingipain and lys-gingipains are responsible for this proteolysis. In a study using a mouse model, "P. gingivalis" was specifically found to down-regulate IL-8 induction, causing delayed neutrophil recruitment. Prevention of neutrophil recruitment may inhibit the clearance of the bacterium from the site of infection allowing for colonization. "P. gingivalis" is able to evade opsonophagocytosis from PMN’s by using Gingipain K (Kgp) to cleave IgG 1 and 3. This further modulates immune response by impairing signaling. Other studies have found that "P. gingivalis" can subvert the complement pathway through C5αR and C3αR, which modulates the killing capacity of leukocytes, allowing for uncontrolled bacterial growth. "P. gingivalis" was also found to inhibit pro inflammatory and antimicrobial responses in human monocytes and mouse macrophages by fimbrial binding to CXCR4, inducing PKA signaling and inhibiting TLR-2-mediated immune response.