Immuno-colocalization of IRF5 with TRAF6 and AKT2 in Human Apical Periodontitis
Immuno-colocalization of IRF5 with TRAF6 and AKT2 in Human Apical Periodontitis
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IRF5 与 TRAF6 和 AKT2 在人根尖周炎中的免疫共定位
DOI：
10.1016/j.joen.2022.03.003
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发表时间：
2022
影响因子：
4.2
通讯作者：
Bin Peng
中科院分区：
文献类型：
--
作者：
Jingjing Yu;Huan Zhao;Guojing Liu;Lingxin Zhu;Bin Peng
干扰素调节因子5（IRF 5）对于健康和疾病中的免疫和炎症反应的调节至关重要。然而，IRF 5在人类根尖牙周炎中的存在仍然未知。为探讨IRF 5、肿瘤坏死因子受体相关因子6（TRAF 6）和AKT 2在根尖周炎组织中的表达及共定位，选取39例根尖周组织，包括健康牙龈组织（n = 12）、根尖肉芽肿组织（n = 13）和根尖囊肿（n = 14）。苏木精-伊红染色观察病灶内炎性浸润情况。免疫组化法检测IRF 5的表达。进行双重免疫荧光评估以分别将IRF 5与CD 68、TRAF 6和AKT 2共定位。免疫组化结果显示IRF 5在PGs和RC中的表达均显著高于健康对照组。与健康对照组相比，RCs和PG中IRF 5-CD 68双阳性细胞占优势。IRF 5-TRAF 6和IRF 5-AKT 2双阳性细胞在根尖周病变组织中的表达与健康对照组织相比差异有统计学意义; IRF 5在人根尖周组织巨噬细胞中高表达，并与TRAF 6和AKT 2共定位。这些发现可能为理解根尖周病的发病机制提供新的线索。
Interferon regulatory factor 5 (IRF5) is critical for the regulation of immune and inflammatory responses in health and diseases. However, the presence of IRF5 in human apical periodontitis remains unknown. This study aimed to explore the expression and colocalization of IRF5 with tumor necrosis factor receptor-associated factor 6 (TRAF6) and AKT2 in human apical periodontitis.A total of 39 human periapical tissues, including healthy gingival tissues (n = 12), periapical granulomas (PGs, n = 13), and radicular cysts (RCs, n = 14), were used in this study. The inflammatory infiltrates of lesions were evaluated by hematoxylin-eosin staining. The expression of IRF5 was detected by immunohistochemistry. Double immunofluorescence assessment was performed to colocalize IRF5 with CD68, TRAF6, and AKT2, respectively. Data were analyzed using the Kruskal-Wallis test.Immunohistochemistry revealed significantly higher expressions of IRF5 in PGs and RCs than the healthy control group. IRF5-CD68 double-positive cells were more predominant in RCs and PGs than the healthy control group. Significant differences of the IRF5-TRAF6 and IRF5-AKT2 double-positive cells were detected in periapical lesions compared with the healthy control tissues.IRF5 was highly expressed in macrophages of human periapical tissues and was colocalized with TRAF6 or AKT2 in human periapical tissues. These findings may provide new clues for understanding the pathogenesis of periapical diseases.