Abstract
Recent investigations into the regulation of the inflammation in the periodontitis have revealed that chronic inflammatory diseases such as periodontitis are characterized by an imbalance in the proinflammatory and proresolution mediators and can be characterized by a failure of the resolution pathways in the late stages of the acute inflammatory response. The proresolution mediators, termed as specialized proresolving mediators (SPMs), comprise the lipoxins, resolvins, protectins, and maresins that are derived from the arachidonic acid or omega-3 polyunsaturated fatty acids. In the animal studies, treatment of the periodontitis with the topical SPMs return the inflammatory lesion to the homeostasis with the regeneration of all the components of the periodontal organ lost to the disease. In this article, the study investigates the immunomodulatory role of SPMs in the periodontal ligament stem cells (PDLSCs). Primary porcine PDLSCs (pPDLSCs) were stimulated with interleukin-1β (IL-1β) and interleukin-17 (IL-17) in vitro to simulate the periodontal inflammation in the presence or absence of SPMs. This study found that IL-1β and IL-17 synergistically activated the proinflammatory genes of pPDLSCs and altered the immune phenotype of pPDLSCs including the key signaling pathways. Addition of SPMs rescued the pPDLSCs phenotype and induced further production of the additional SPMs, which was reflected by upregulation of the requisite enzymes 12- and 15-lipoxygenase by pPDLSCs. This study interrogated the immunomodulatory actions of pPDLSCs on the monocytes/macrophages, focusing on the porcine CD14/CD16/CD163 markers by using flow cytometry. This study utilized the CD14+CD16+/CD14+CD16− ratio and CD163 on the monocytes/macrophages to differentiate between a proinflammation phenotype (lower ratio) and a resolution of the inflammation phenotype (higher ratio). This study also found that the conditioned medium from pPDLSCs treated with the cytokines and Maresin1 increased the CD14+CD16+/CD14+CD16− ratio and had the highest CD163 expression. This study concludes that in an inflammatory environment, pPDLSCs become proinflammatory and exert immunomodulatory functions. Maresin 1 resolves the inflammation by acting on pPDLSCs directly and by shifting the monocytes/macrophages phenotype to the proresolution dominance.
Highlights
Periodontitis and peri-implantitis are the inflammatory diseases that are initiated by the bacteria [1]
Resolution of the inflammation is driven by a group of specialized proresolving mediators (SPMs) comprising the lipoxins, resolvins, protectins, and maresins that are derived from the arachidonic acid or omega3 polyunsaturated fatty acids (PUFAs) [4]
We confirmed the stem/stromal cell properties of the isolated porcine PDLSCs (pPDLSCs) by the flow cytometry and differentiation assays
Summary
Periodontitis and peri-implantitis are the inflammatory diseases that are initiated by the bacteria [1]. Recent investigations into the regulation of the inflammation in the periodontitis have revealed that the chronic inflammatory diseases such as periodontitis are characterized by an imbalance in the proinflammatory and proresolution mediators and can be characterized by a failure of the resolution pathways in the late stages of the acute inflammatory response [2, 3]. Resolution of the inflammation is an active process in which SPMs interact with their respective receptors on the cells to halt the neutrophil influx, skew monocytes/macrophages toward the M2-like phenotype with increased phagocytosis, and to limit the adaptive immune activation [5]. These actions lead to a well-orchestrated quick return to the immune homeostasis. Administration of exogenous SPMs in pathological inflammatory lesions breaks the cycle of the chronicity and facilitates the return to the physiological form and function [5]
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