Centre of Neuroscience of Milan, Department of Medicine and Surgery, University of Milan, 20122 Milano, Italy.
Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy.
Int J Mol Sci. 2022 Oct 31;23(21):13242. doi: 10.3390/ijms232113242.
Much evidence suggests autoimmunity in the etiopathogenesis of periodontal disease. In fact, in periodontitis, there is antibody production against collagen, DNA, and IgG, as well as increased IgA expression, T cell dysfunction, high expression of class II MHC molecules on the surface of gingival epithelial cells in inflamed tissues, activation of NK cells, and the generation of antibodies against the azurophil granules of polymorphonuclear leukocytes. In general, direct activation of autoreactive immune cells and production of TNF can activate neutrophils to release pro-inflammatory enzymes with tissue damage in the gingiva. Gingival inflammation and, in the most serious cases, periodontitis, are mainly due to the dysbiosis of the commensal oral microbiota that triggers the immune system. This inflammatory pathological state can affect the periodontal ligament, bone, and the entire gingival tissue. Oral tolerance can be abrogated by some cytokines produced by epithelial cells and activated immune cells, including mast cells (MCs). Periodontal cells and inflammatory-immune cells, including mast cells (MCs), produce cytokines and chemokines, mediating local inflammation of the gingival, along with destruction of the periodontal ligament and alveolar bone. Immune-cell activation and recruitment can be induced by inflammatory cytokines, such as IL-1, TNF, IL-33, and bacterial products, including lipopolysaccharide (LPS). IL-1 and IL-33 are pleiotropic cytokines from members of the IL-1 family, which mediate inflammation of MCs and contribute to many key features of periodontitis and other inflammatory disorders. IL-33 activates several immune cells, including lymphocytes, Th2 cells, and MCs in both innate and acquired immunological diseases. The classic therapies for periodontitis include non-surgical periodontal treatment, surgery, antibiotics, anti-inflammatory drugs, and surgery, which have been only partially effective. Recently, a natural cytokine, IL-37, a member of the IL-1 family and a suppressor of IL-1b, has received considerable attention for the treatment of inflammatory diseases. In this article, we report that IL-37 may be an important and effective therapeutic cytokine that may inhibit periodontal inflammation. The purpose of this paper is to study the relationship between MCs, IL-1, IL-33, and IL-37 inhibition in acute and chronic inflamed gingival tissue.
大量证据表明自身免疫在牙周病的发病机制中起作用。事实上，在牙周炎中，会产生针对胶原蛋白、DNA 和 IgG 的抗体，以及增加的 IgA 表达、T 细胞功能障碍、炎症组织中牙龈上皮细胞表面 II 类 MHC 分子的高表达、NK 细胞的激活以及针对多形核白细胞嗜天青颗粒的抗体的产生。一般来说，自身反应性免疫细胞的直接激活和 TNF 的产生可以激活中性粒细胞，导致牙龈组织损伤中促炎酶的释放。牙龈炎症，在最严重的情况下，牙周炎，主要是由于共生口腔微生物群落的失调触发了免疫系统。这种炎症病理状态会影响牙周韧带、骨骼和整个牙龈组织。上皮细胞和激活的免疫细胞产生的一些细胞因子，包括肥大细胞 (MCs)，可以破坏口腔耐受。牙周细胞和炎症免疫细胞，包括肥大细胞 (MCs)，产生细胞因子和趋化因子，介导牙龈的局部炎症，同时破坏牙周韧带和牙槽骨。炎症细胞因子，如 IL-1、TNF、IL-33 和细菌产物，包括脂多糖 (LPS)，可以诱导免疫细胞的激活和募集。IL-1 和 IL-33 是白细胞介素 1 家族成员的多效细胞因子，它们介导 MCs 的炎症，并有助于牙周炎和其他炎症性疾病的许多关键特征。IL-33 激活几种免疫细胞，包括淋巴细胞、Th2 细胞和固有和获得性免疫疾病中的 MCs。牙周炎的经典治疗方法包括非手术牙周治疗、手术、抗生素、抗炎药和手术，但仅部分有效。最近，一种天然细胞因子，白细胞介素 37（IL-37），一种白细胞介素 1 家族成员和白细胞介素 1b 的抑制剂，因其治疗炎症性疾病而受到广泛关注。在本文中，我们报告称，IL-37 可能是一种重要且有效的治疗性细胞因子，可抑制牙周炎症。本文的目的是研究 MCs、IL-1、IL-33 和 IL-37 抑制在急性和慢性炎症性牙龈组织中的关系。
