Fig 2: The keratinocyte-targeted lipid-polymer nanohybrids downregulate IMQ-induced NF-?B activation leading to the decrease of cytokine and chemokine expression of psoriasis-like skin. The protein expression of (A) IFN-?, (B) IL-1ß, (C) IL-6, (D) IL-17A, (E) IL-17E, (F) IL-22, (G) IL-23, (H) TNF-a, (I) CXCL1, and (J) CXCL2 in IMQ-induced psoriatic skin. (K) Representative IHC staining for p-NF-?B. Scale bars, 100 µm. (L) Immunoblotting analysis with p-NF-?B. DSC, desmocollin; DP, desmoplakin; PG, plakoglobin; PP, plakophilin. Data are expressed as mean ± SEM (n=4). P < 0.05, ** P < 0.01, *** P < 0.001, compared with control group.

Fig 3: Associations between CXCLs and OS in patients with colorectal cancer. Comparison of OS between patients with high and low (A) CXCL1, (B) CXCL2, (C) CXCL8, (D) CXCL13 and (E) CXCL14 expression. OS, overall survival; CXCL, C-X-C motif chemokine ligand.

Fig 4: Induction of chemokine (C-X-C motif) ligand 8/macrophage inflammatory protein-2 (CXCL8/MIP-2) by lugdunin is TLR2/MyD88-dependent. a HEK-control or HEK-TLR2 cells were treated with 2 µM lugdunin for 5 h and subsequently the CXCL8 concentration in the supernatant was analyzed by LEGENDplexTM (BioLegend). Shown is one representative experiment of three independent experiments with two technical replicates ± s.e.m. b HEK-control or HEK-TLR2 cells were treated with increasing concentrations of lugdunin for 5 h and subsequently expression of CXCL8 was analyzed and normalized to actin. Shown is one representative experiment of three independent experiments with two technical replicates ± s.e.m. c Schematic overview of the mouse experiments: 6–8-week-old female C5BL/6 WT, MyD88-knockout (ko), or 5xTLR-ko mice were epicutaneously treated with 1.5 µg lugdunin or phosphate-buffered saline (PBS) as a control. After 24 h, mice were euthanized, 4 mm skin punches were taken, and further cultured in vitro for 10 h followed by cytokine analysis of the culture supernatant by LEGENDplexTM (BioLegend). d, e Shown are the mean concentrations of IL-1a (d) or MIP-2 (e) in the skin culture supernatant of two skin punches from four mice each ± s.e.m. Significant differences to control treatments were analyzed by an unpaired two-tailed t test (*P < 0.05; **P < 0.01; ***P < 0.001). f Representative MIP-2-stained paraffin-embedded mouse skin sections. Scale bar, 100 µM. Source data are provided as a Source Data file

Fig 5: Adenine-induced CKD mice exhibit lung inflammation. (a) Serum creatinine and BUN levels, (b) serum phosphate and FGF23 levels, and (c) total cell count and macrophage, lymphocyte, and neutrophil counts from BAL fluid of mice on the adenine diet and littermates on the control diet. Left y-axis applies to total cell and macrophage count; right y-axis applies to lymphocyte and neutrophil count. (d) Representative pathology of IL1B and CXCL2 IHC-stained lung sections (scale bar, 100 µM) from mouse lungs of both groups. (e) Relative mRNA transcript levels of Il1b and Cxcl2 in total mouse lung homogenates. All values are mean ± SEM with *p = 0.05, **p < 0.01, and ***p < 0.001 and n = 10 mice/group. Statistical significance was analyzed via unpaired Student’s t-test (a–e).