State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
J Endod. 2018 Aug;44(8):1276-1282. doi: 10.1016/j.joen.2018.04.015. Epub 2018 Jun 20.
Interferon regulatory factor 8 (IRF8) is a critical transcription factor in innate immune responses that regulates the development and function of myeloid cells. Human periapical lesions are caused by endodontic microbial infections. However, the presence of IRF8 in human periapical lesions remains elusive. This study aims to explore the expression of IRF8 in human periapical lesions and the possible association of IRF8 with macrophages, nuclear factor kappa B (NF-κB) signaling, and the autophagy process.
Thirty-nine human periapical tissues, including healthy control tissues (n = 15), radicular cysts (RCs, n = 11), and periapical granulomas (PG, n = 13), were examined. Tissues were fixed in paraformaldehyde and analyzed. The inflammatory infiltrates of lesions were evaluated by hematoxylin-eosin, and the expression of IRF8 was analyzed by immunohistochemistry. Double immunofluorescence assessment was performed to colocalize IRF8 with CD68, NF-κB p65, and LC3B.
The expression of IRF8 was significantly higher in RCs and PGs than in the healthy control group, but no significant difference was found between RCs and PGs. There were significantly more IRF8-CD68 double-positive cells in RCs and PGs than in the healthy control group, but no significant difference was observed between RCs and PGs. Double-labeling analysis of IRF8 with NF-κB and LC3B indicated that IRF8 expression is associated with NF-κB signaling and the autophagy process during periapical lesions.
IRF8 could be observed and might possibly be involved in macrophages in the development of periapical lesions.
干扰素调节因子 8（IRF8）是先天免疫反应中的关键转录因子，调节髓样细胞的发育和功能。人根尖周病变是由牙髓微生物感染引起的。然而，IRF8 在人根尖周病变中的存在仍然难以捉摸。本研究旨在探讨 IRF8 在人根尖周病变中的表达，以及 IRF8 与巨噬细胞、核因子 kappa B（NF-κB）信号转导和自噬过程的可能关联。
检查了 39 个人根尖周组织，包括健康对照组（n=15）、根尖囊肿（RC，n=11）和根尖肉芽肿（PG，n=13）。组织用多聚甲醛固定并进行分析。通过苏木精-伊红染色评估病变的炎症浸润，通过免疫组织化学分析 IRF8 的表达。进行双重免疫荧光评估以将 IRF8 与 CD68、NF-κB p65 和 LC3B 共定位。
RC 和 PG 中的 IRF8 表达明显高于健康对照组，但 RC 和 PG 之间无显著差异。RC 和 PG 中的 IRF8-CD68 双阳性细胞明显多于健康对照组，但 RC 和 PG 之间无显著差异。IRF8 与 NF-κB 和 LC3B 的双重标记分析表明，IRF8 表达与根尖周病变过程中的 NF-κB 信号转导和自噬过程有关。
在根尖周病变的发展过程中，可以观察到 IRF8，并且可能涉及巨噬细胞。
