Table 1.

Mechanisms and consequences of Porphyromonas gingivalis causing subversion of polymorphonuclear leukocytes

Mechanisms	Consequences	Refs
Whole cells, LPS bind to adhesion molecules (IL-8, ICAM-1, E-selectin).	Impaired recruitment	(4, 5, 17, 20, 22–28)
SerB suppression of IL-8 production by dephosphorylation of the Ser536 of NF-κB p65 preventing nuclear translocation and transcription.	IL-8 production suppressed	(18, 25, 29, 30)
Bacterial binding to FMLP and PPAD-citrullinated C5a.	Reduced chemotaxis	(17, 19, 31–33, 38, 39, 42)
Dual regulation of TREM-1 by Arg- and Lys-gingipain. Outcome depends on infection stage.	Evasion of host defense	(43)
Resistance to killing by granular contents.	Killing prevented	(33, 40, 41, 45–48, 51, 52)
C5 convertase-like activity produces	Inhibits antimicrobial response	(17, 47, 53, 60)
C5a, which is involved in subversion of C5aR–TLR2 crosstalk. This leads to My88D degradation, PI3K activation and inhibition of RhoA GTPase.	and promotes inflammatory response
Activated CR3 interacts with P. gingivalis fimbriae and induces downregulation of IL-12p70 – a key cytokine in intracellular bacterial clearance.	Reduced bacterial clearance	(61, 62)
LPS and lipid A delay neutrophil apoptosis through TLR2 signaling.	Prolongs acute inflammation	(64–67)

CR3, complement receptor 3; FMLP, N-formyl-methionyl-leucyl-phenylalanine; LPS, lipopolysaccharide; PPAD, peptidylarginine deiminase; TLR2, toll-like receptor 2; TREM-1, triggering receptor expressed on myeloid cells 1.