Figure 1.

Immune responses to pathogens. During an infection with pathogens, for example E. coli, lipopolisaccharide enhances the secretion of chemotactic IL-8 and stimulates the upregulation of E- or P-selectins expression on gingival endothelial cells (GECs). Selectins facilitate neutrophils adhesion during transmigration as they interact with PSGL-1 expressed on PMNs. Moreover, the presence of microbes and their particles activates the complement cascade. C3a and C5a are anaphylatoxins with a strong chemotactic and pro-inflammatory potential. IgG and IgM antibodies or C3b recognize bacterial antigens and opsonize invading pathogens thus facilitating bacterial phagocytosis. LPS activates the TLR4 signaling pathway in recruited neutrophils, eliciting strong inflammatory responses designed to inactivate the pathogen. Inflammatory responses include the production of reactive oxygen species, secretion of pro-inflammatory cytokines and antimicrobial enzymes or peptides, such as cathepsin G, elastase, cathelicidins or defensins. After a successful bacterial clearance, neutrophils undergo apoptosis, an essential process triggering the resolution of inflammation.