Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?

Figure 5

Macrophage polarization in periodontitis. Macrophages that have been found in the gingival epithelium can be activated by several microorganisms able to induce macrophage polarization toward M1- or M2-like phenotype. P. gingivalis releases LPS, IL-1, and TNF-α that promote the proinflammatory M1 macrophage polarization (A). Moreover, Pg infection enhances the secretion of IL-1β, IL-6, IL-12, TNF-α, G-CSF, GM-CSF, and the chemokines eotaxin, MCP1, MIP-1α, and MIP-1β from macrophages, reflecting a M1-like proinflammatory response (B). In spite of this, it has also been reported that Pg infection can also be associated with the increase of IL10, supporting M2 macrophage and increasing arginase-1 production and collagen deposition, leading to periodontitis (C). T. forsythia releases BspA and other ligands that induce TLR2 signaling favouring the development of Th2-type inflammatory responses (D). T. denticola induces TLR2 signaling that stimulates the prolonged activation of both ERK1/2 p38 and JNK1/2 in monocytes (E).