In addition, systemic cytokine/chemokine responses can be identified in patients with periodontitis [3–5]. Interleukin (IL)-1β, tumour necrosis factor (TNF)-α and IL-6 are principal pro-inflammatory cytokines with pleotropic biological activities on immune and non-immune cells, as well as in osteogenic pathways). IL-8 (CXCL8) is the major neutrophil chemokine, while macrophage chemotactic protein (MCP)-1 (CCL2), a major chemoattractant and maturation signal for macrophages, and regulated upon activation, normal T cell expressed and secreted (RANTES; CCL5) is a member of the IL-8 superfamily of cytokines.
It is a selective attractant for memory T lymphocytes and monocytes. These chemokines have all been detected in the serum of patients with microbial infections [6–10], including periodontitis [11–14]. learn more However, chronic stimulation of these biomolecules generally represents dysregulated responses, and is associated frequently with systemic disease sequelae [15–21]. In some cases, particularly with polymicrobial infections at mucosal surfaces, innate immune mechanisms may function exceptionally well to manage surface colonization by commensal opportunistic pathogens and maintain homeostasis [22–25]. Nevertheless, with respect to a number of chronic inflammatory diseases, the interaction between Galunisertib cell line the challenge (e.g. bacteria) and
the inflammatory and innate immune response can result in collateral damage of the local tissues. Adverse pregnancy outcomes provide a potential example of these ramifications of a dysregulated
host response. Ascending vaginal infections trigger the local production of various inflammatory mediators and matrix metalloproteinases (MMP), resulting in amnionitis that impact placental functions negatively and lead potentially to fetal infection [26–32]. Reports described relationships between the presence of inflammatory mediators in amniotic fluid and uterine contractions and/or birth in humans and non-human primates. Proinflammatory cytokines/chemokines, immunomodulatory and immunosuppressive IKBKE cytokines and prostanoids [e.g. prostaglandin E2 (PGE2)] are produced by the amniotic and decidual membranes and can be found in fetal circulation and amniotic fluid, often associated with premature delivery. Expanding literature supports that the levels of many of these cytokines/chemokines in serum are also reflective of, and potentially contribute to, the risk for premature rupture of membranes (PROM) with preterm labour and delivery [26,32–35]. Consequently, relationships between serum and local cytokine levels and their association with adverse pregnancy outcomes are possible. Periodontitis is a chronic oral infection with polymicrobial biofilms triggering a localized immunoinflammatory lesion.