ArticleJournal of inflammation research2025
IRF3 Promotes Production of IL-6 and Nitric Oxide but Represses CCL22 in RAW264.7 Macrophage Cells Exposed to Lipopolysaccharides in Culture.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: 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 Results: Herein, LPS of 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.
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