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Human cells challenged with microorganisms influence their environment for example
via interleukin secretion. The response strongly depends on the specific cell type,
microbial species, abundance or composition of the resident microbiome as well as on
host environment factors. Healthy patients, hence periodontium without signs of
inflammation, have a balanced host – microbial interaction (Marsh, 2006; Tribble &
Lamont, 2010). Biofilm maturation and colonization of bacteria associated with
periodontal disease alter the composition of biofilms, enhance interaction with host
cells directly or via virulence factors (Lamont et al., 1992), and thereby provoke
inflammatory responses. Diseased periodontal tissues show a distinct miRNA expression
profile which differs fundamentally from healthy periodontal cells (Lee et al., 2011;
Nahid et al., 2011; Xie et al., 2011; Kagiya & Nakamura, 2013). These miRNAs, small noncoding
RNAs with regulatory function, are involved in several processes, e.g.,
differentiation, proliferation, TLR recognition, immune modulation via chemokines and
apoptosis.
Inflammatory environments are characterized by high levels of pro-inflammatory
cytokines which attract PMNs and enhance tissue infiltration of immune cells (Attstrom
& Egelberg, 1970). The antimicrobial activities of PMNs apart from phagocytosis and
NETosis, e.g., release of antimicrobial peptides and reactive oxygen species, are crucial
in the reduction of biofilm development (Darveau et al., 1997). Patients with deficiencies
in PMN activity or reduced numbers show more progressive tissue degradation,
indicating the role of PMNs in microbial challenges (Dennison & van Dyke, 1997).
Nevertheless, PMN activity is a major initiator of tissue degradation (Liu et al., 2001).
Survival of PMNs is influenced by the environmental settings. Lakschevitz and colleagues
(2013) demonstrated prolonged PMN survival in individuals suffering from periodontitis,
and hypoxic conditions led to similar effects (Hannah et al., 1995). The level of PMN
apoptosis was restored under hypoxia when PMNs were incubated with inhibitors of the
mitogen-activated protein kinases (MAPK), which indicates that MAPK signaling is
relevant in PMN survival in hypoxic environment, most likely via induction of the antiapoptotic
protein Mcl-1 (Leuenroth et al., 2000). MAPK are also involved in osteogenesis
of periodontal stem cells (Yu et al., 2012), affect interleukin secretion of periodontal
cells (Kirkwood & Rossa, 2009; Murayama et al., 2011), and the inhibition of MAPK has
protective effects against bone loss in a rat periodontitis model (Kirkwood et al., 2007;
Rogers et al., 2007)

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