Fig. 2: IPANP reprograms myeloid cells toward the pro-inflammatory macrophage phenotype.

a Schematic representation of inducing macrophage repolarization from M2 to M1 phenotype through incubating BMDMs with different formulations. Created in BioRender. Zonghe, L. (2026) https://BioRender.com/48gbeau. b miR-182 expression in M0/M1/M2 BMDMs (n = 3 biological independent samples). c Expression heatmap of the up- and downregulated miRNAs in the human M2 versus M0, M1 macrophages (GSE51307). d Kaplan–Meier analysis of overall survival of miR-182. e Western blot analysis on the expression of Arg1 and iNOS in the repolarized macrophages from M2 BMDMs (n = 3 biological independent samples). f–i The expression of TGF-β, IL-10, TNF, and IL-12 determined by ELISA (n = 3 biological independent samples). j–m Representative images of flow cytometry and quantification of the expression of CD206 (M2 phenotype) and CD86 (M1 phenotype) in BMDMs after different treatments (n = 3 biological independent samples). n Volcano map of expressed differentially genes between the PBS group and the IPANP + laser group. o Expression heatmap of M2 and M1-macrophage marker genes of BMDMs treated with different formulations. p–r Signaling pathway enrichment analysis of Kyoto Encyclopedia of Genes and Genomes (KEGG) in IPANP + laser treated BMDMs. s TLR4 and MYD88 expression and P65 phosphorylation in BMDMs treated with different formulations (n = 3 biological independent samples). Statistical significance was determined using one-way ANOVA with Tukey’s multiple comparison tests in (b, f–i, k–m), and log-rank tests in (d). DEGs were analysed using DESeq2 (two-sided Wald test) (n). KEGG pathway enrichment (q, r) were performed based on DESeq2 results. The results are presented as mean ± standard deviation (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001). Source data are provided as a Source data file.