ArticlePloS one2026
IL15.3, a synthetic antimicrobial peptide, attenuates LPS-induced inflammatory responses in RAW 264.7 macrophages via transcriptional and proteomic modulation.
Article in PloS one, 2026. 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
Inflammation underlies numerous pathological conditions, driving the need for safe and effective anti-inflammatory agents. Anti-inflammatory peptides (AIPs) are promising therapeutics due to their specificity, efficacy, and safety. This study evaluated the cationic antimicrobial peptide IL15.3 for anti-inflammatory activity and cytocompatibility in vitro. IL15.3 demonstrated low cytotoxicity in MTT assays using RAW 264.7 macrophages, normal human dermal fibroblasts (NHDF), and HaCaT keratinocytes. In LPS-stimulated RAW 264.7 cells, IL15.3 significantly reduced nitric oxide (NO) production and reactive oxygen species (ROS) in a dose-dependent manner without affecting cell viability. qRT-PCR analysis revealed significant suppression of iNOS, COX-2, TNF-α, and IL-6 mRNA expression, alongside downregulation of NF-κB, JNK, STAT1, and STAT3, and a reciprocal shift in Keap1/Nrf2 expression suggestive of possible antioxidant pathway activation. Label-free proteomic profiling identified 5,191 proteins, revealing a multi-modal mechanism of action. IL15.3 treatment exclusively induced 4 anti-inflammatory proteins (ISG15, PEX14, TNIP3, PR) and upregulated negative regulators NRG1, DAB2IP, IL-18BP and SOCS5. Critically, IL15.3 suppressed key pro-inflammatory mediators including IKKβ, JAK1, JAK3, JNK, and IL-1RAcP, demonstrating comprehensive modulation of NF-κB, JAK/STAT, and MAPK pathways. In silico molecular docking further predicted potential interactions of IL15.3 with iNOS and the Keap1 Kelch domain, offering preliminary structural insight consistent with its putative dual anti-inflammatory and antioxidant activity. Together, these findings indicate that IL15.3 exhibits potent anti-inflammatory and antioxidant activity through multiple mechanisms in LPS-stimulated macrophages at transcriptional and proteomic levels. The coordinated upregulation of negative regulators and suppression of central inflammatory mediators collectively suggest that IL15.3 may represent a promising therapeutic candidate for inflammatory disorders.
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