, 2008). This could well constitute a mechanism of expansion of the periodontal pocket epithelium, which is a histopathological
feature of periodontitis. It is now well established that P. gingivalis is not an aggressor of the inflammatory response, but rather an opportunist that can cross-talk with the host and subvert its defence mechanisms. Using this strategy, P. gingivalis prolongs its survival and becomes established in the periodontal pocket (Hajishengallis et al., 2011). It preferentially deregulates innate immunity, which may in turn disable adaptive immunity (Hajishengallis, 2009; Pathirana et al., 2010). Important representative examples of these abilities are its capacity to degrade human defensins Selleck ABT-263 (Carlisle et al., 2009), its resistance to oxidative selleck screening library burst-killing by polymorphonuclear neutrophils (PMNs) (Mydel et al., 2006) and its ability to inhibit ‘at will’ the production of crucial proinflammatory cytokines (Bostanci et al., 2007a, b). Although P. gingivalis has the capacity to stimulate interleukin (IL)-8 production by epithelial cells (Sandros et al., 2000; Asai et al., 2001; Kusumoto et al., 2004), it can also inhibit IL-8 production, resulting in hindered PMN chemotaxis, a phenomenon known as ‘chemokine paralysis’ (Darveau et al., 1998). Porphyromonas gingivalis thereby incapacitates the first line of
defence in the periodontal tissues. Moreover, by inhibiting IL-12
production by macrophages, it prevents cytotoxic T-cell activation and therefore bacterial clearance (Hajishengallis et al., 2007). Accordingly, by inhibiting interferon (IFN)-γ production by T cells, it inhibits macrophage bacteriocidal activity Liothyronine Sodium and hence bacterial clearance (Pulendran et al., 2001; Hajishengallis et al., 2007). A special relationship is also revealed between P. gingivalis and the complement system, as it can suppress its activation, that is by degradation of C3 and capturing of C4b-binging protein, but also by synergizing with C5a via exploiting toll-like receptor (TLR)-2 signalling (Wang et al., 2010). A further interesting point is that whole viable P. gingivalis is differentially sensed by the host, compared with its released virulence factors, with the potential to activate distinctive intracellular pathways (Pathirana et al., 2010), or differential cytokine production (Zhou et al., 2005). As an opportunistic pathogen, it is not surprising that P. gingivalis possesses a number of virulence factors. These are molecules that can elicit deleterious effects on host cells, essentially the survival ‘weapons’ of P. gingivalis. The main virulence factors discussed here are LPS, capsular polysaccharide (CPS), fimbriae and gingipains. Like all Gram-negative bacterial species, P.