ArticleJournal of inflammation (London, England)2025
Unveiling the anti-inflammatory potential of RF16, an interleukin 8-derived therapeutic peptide in macrophages.
Article in Journal of inflammation (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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5 authors.
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Abstract
backgroundInterleukin 8 (IL-8, also known as CXCL-8) regulates inflammation and breast cancer formation by activating its cognate receptor CXCR1/2. In our previous study, a RF16 peptide, derived from the IL-8 binding region of CXCR1/2, was synthesized to inhibit IL-8-stimulated and LPS-induced adhesion and transmigration of monocytes. However, the anti-inflammatory effects of RF16 on THP-1 cells remain unknown.
methodsTHP-1 cells were differentiated with PMA overnight, followed by an one hour pretreatment of the IL-8 antagonist peptide RF16. IL-8 or TNF-α was then added for further incubation. The supernatant, mRNA, and protein of the cells were harvested. The secretion of TNF-α, IL-1β, and IL-6 was measured, along with assessment of ROS production and oxLDL uptake. Protein expression of different signaling pathways was analyzed. RF16 was also treated in a mouse model of acute sepsis to evaluate the white blood cell (WBC) count and serum IL-6 levels.
resultsOur results indicate that RF16 was able to reduce mRNA and protein expression of inflammatory cytokines including TNF-α, IL-8, IL-6, and IL-1β levels in TNF-α/IL-8-induced THP-1 cells, with some results showing a dose-dependent trend. We found that RF16 was able to inhibit TNF-α/IL-8-induced ROS generation, thereby suppressing the inflammatory response. Moreover, a higher concentration (1 uM) of RF16 can alleviate oxLDL uptake induced by TNF-α and IL-8. Further investigation revealed that NF-κB, PI3K, and MAPK signaling pathways were the main mechanism responsible for the inhibition of inflammation. In addition, using the LPS-induced sepsis animal model, RF16 was able to reduce the number of white blood cells in peripheral blood, and subsequently reduce IL-6 levels.
conclusionOur results demonstrated that RF16 has the ability to suppress the expressions and secretions of TNF-α, IL-8, and LPS-induced pro-inflammatory cytokines in both in vitro and in vivo.
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