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Comment
. 2018 Sep;97(10):1079-1081.
doi: 10.1177/0022034518785857. Epub 2018 Jul 11.

Macrophages: The Bridge between Inflammation Resolution and Tissue Repair?

G P Garlet  1 , W V Giannobile  2   3   4
Affiliations
Comment

Macrophages: The Bridge between Inflammation Resolution and Tissue Repair?

G P Garlet et al. J Dent Res. 2018 Sep.
No abstract available

Keywords: bone tissue; immunology; periodontal; periodontitis; regeneration; wound healing.

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Conflict of interest statement

The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.

Figures

Figure.
Figure.
Schematic representation of the potential role of macrophages as a bridge between inflammation resolution and tissue repair. In the periodontal environment, the presence of periodontopathogens and its products (such as lipopolysaccharide) is assumed to drive an initial polarization of M0 macrophages toward the M1 phenotype. M1 macrophages are a characteristic source of proinflammatory cytokines, such as tumor necrosis factor (TNF), which present a key role in the development of inflammatory immune reaction in periodontal tissues. The subsequent migration of certain Th subsets, such as Th1 and Th17 cells, can independently boost the inflammatory process. Th1 cells are described to have an interesting interplay with the M1 subset, since M1 cells can produce interleukin (IL)–12, enhancing Th1 polarization, and Th1 cells are the prototypic source of interferon (IFN) γ, which contribute to M1 phenotype acquisition. Taken together, such cellular elements contribute to a sustained and exacerbated host response, resulting in a local milieu characterized by increased proteolytic and osteoclastogenic pathways, linking the tissue breakdown outcome as a result of the “destructive inflammation.” On the other hand, the conversion of M1 macrophages toward a M2 phenotype, which can be mediated by IL-4, can result in a switch of the overall environment. M2 macrophages can produce anabolic and anti-inflammatory factors such as transforming growth factor (TGF) β and IL-10; coincidentally, the same cytokines are characteristically produced by Tregs. The production of such cytokines can boost both M2 and Treg activity and consequently counteract the “destructive inflammation.” Th2 cells can also contribute to the local immunoregulation by mediating Treg infiltration via the IL-4/CCL22/CCR4 axis. Interestingly, the putative cooperative activity of Th2, Treg, and M2 cells would be responsible for shutting down the chronic inflammatory osteolytic stimuli and also for triggering tissue repair via elements such as CysC, characterizing a constructive inflammation environment.
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