Academic Journal
IRF3 Promotes Production of IL-6 and Nitric Oxide but Represses CCL22 in RAW264.7 Macrophage Cells Exposed to Lipopolysaccharides in Culture
العنوان: | IRF3 Promotes Production of IL-6 and Nitric Oxide but Represses CCL22 in RAW264.7 Macrophage Cells Exposed to Lipopolysaccharides in Culture |
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المؤلفون: | Moore TC, Pinkerton TS, Petro TM |
المصدر: | Journal of Inflammation Research, Vol Volume 18, Pp 1255-1265 (2025) |
بيانات النشر: | Dove Medical Press, 2025. |
سنة النشر: | 2025 |
المجموعة: | LCC:Pathology LCC:Therapeutics. Pharmacology |
مصطلحات موضوعية: | irf3, lipopolysaccharide, macrophages, raw264.7 cells, cytokines, Pathology, RB1-214, Therapeutics. Pharmacology, RM1-950 |
الوصف: | Tyler C Moore,1 Terrence Scott Pinkerton,1 Thomas M Petro2 1Department of Biology, College of Science and Technology, Bellevue University, Bellevue, NE, 68005, USA; 2Department of Oral Biology, University of Nebraska Medical Center, Lincoln, NE, 68583, USACorrespondence: Thomas M Petro, Department of Oral Biology, University of Nebraska Medical Center, College of Dentistry, 4000 East Campus Loop South, Lincoln, NE, 68583, USA, Email tpetro@unmc.eduIntroduction: Macrophage responses to lipopolysaccharides (LPS) drive inflammatory diseases, such as periodontitis, with production of IL-6 and Nitric Oxide (NO). However, anti-inflammatory macrophages counter inflammation with the production of CCL22. Interferon regulatory factor 3 (IRF3) plays a significant role in expression of both IL-6 and NO during macrophage responses through Interferon-stimulated Response Elements (ISREs) of promoters.Methods: To determine the role of IRF3 in LPS-induced pro- and anti-inflammatory macrophage responses, we used the macrophage cell line RAW264.7 modified with an ISRE promoter driving secreted luciferase (RAW264.7-Lucia) to assess IRF3 activity in response to Escherichia coli and Porphyromonas gingivalis LPS. For comparison, responses to poly I:C and IFN-gamma and responses from RAW264.7 cells deficient in IRF3 were also assessed.Results: Herein, LPS of P. gingivalis, significantly enhanced production of IL-6 and NO that was induced by E. coli LPS but significantly decreased poly I:C-induced ISRE promoter activity. Moreover, IRF3 deficiency depressed the LPS-induced ISRE promoter activity and NO production but increased IL-6 and CCL22 in response to LPS. Restoration of IRF3 expression in IRF3KO RAW cells increased IL-6, restored NO, and decreased CCL22 production in response to LPS of E. coli.Discussion: Therefore, IRF3 is critical to the expression of pro- and anti-inflammatory factors produced by macrophages responding to LPS and could be a target during periodontitis treatment.Keywords: IRF3, lipopolysaccharide, macrophages, RAW264.7 cells, cytokines |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1178-7031 |
Relation: | https://www.dovepress.com/irf3-promotes-production-of-il-6-and-nitric-oxide-but-represses-ccl22--peer-reviewed-fulltext-article-JIR; https://doaj.org/toc/1178-7031 |
URL الوصول: | https://doaj.org/article/0fbda34f37284b99918e1c052b550fdf |
رقم الانضمام: | edsdoj.0fbda34f37284b99918e1c052b550fdf |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 11787031 |
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