Immunocolocalization of Interferon Regulatory Factory 5 with Tumor Necrosis Factor Receptor–associated Factor 6 and AKT2 in Human Apical Periodontitis

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 fac...

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Veröffentlicht in:Journal of endodontics 2022-06, Vol.48 (6), p.759-767
Hauptverfasser: Yu, Jingjing, Zhao, Huan, Liu, Guojing, Zhu, Lingxin, Peng, Bin
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container_issue 6
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container_title Journal of endodontics
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creator Yu, Jingjing
Zhao, Huan
Liu, Guojing
Zhu, Lingxin
Peng, Bin
description 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.
doi_str_mv 10.1016/j.joen.2022.03.003
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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.</description><identifier>ISSN: 0099-2399</identifier><identifier>EISSN: 1878-3554</identifier><identifier>DOI: 10.1016/j.joen.2022.03.003</identifier><identifier>PMID: 35314291</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>AKT2 ; human apical periodontitis ; IRF5 ; macrophage ; tumor necrosis factor receptor–associated factor 6</subject><ispartof>Journal of endodontics, 2022-06, Vol.48 (6), p.759-767</ispartof><rights>2022 American Association of Endodontists</rights><rights>Copyright © 2022 American Association of Endodontists. 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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. 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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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>35314291</pmid><doi>10.1016/j.joen.2022.03.003</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-5871-0676</orcidid></addata></record>
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subjects AKT2
human apical periodontitis
IRF5
macrophage
tumor necrosis factor receptor–associated factor 6
title Immunocolocalization of Interferon Regulatory Factory 5 with Tumor Necrosis Factor Receptor–associated Factor 6 and AKT2 in Human Apical Periodontitis
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