Fig 1: Systemic infection with a hyperactive STE11ΔN467 mutant attenuates fungal burden in multiple niches within a mouse host.(A) ICR mice were intravenously infected with 1x106 cells of C. albicans wild-type (Day286) or the STE11/Ptet-off-STE11ΔN467 strain and their kidneys, livers, spleens, and brains were harvested 4 days post infection (d.p.i.) to assess fungal burden. (n = 6 mice)(*p<0.05, **p<0.01, ***p<0.0005, ****p<0.0001, by Kruskal-Wallis test with Dunn’s multiple comparisons post-hoc analysis). (B) Serum collected 4 days post infection was assessed to determine the protein concentrations of TNFα, CCL5, CXCL10, IFNα and IL-6 via flow cytometry using the LEGENDplex cytokine bead-based array kit. (n = 8 mice)(*p<0.05, **p<0.005, ***p<0.0005, by Mann-Whitney test).
Fig 2: The weak effect of peramivir on some cytokines in the bronchoalveolar lavage fluid (BALF) of mice. (A, B) BALF cytokines: IFN-γ, IFN-β. (C) BALF chemokines: MCP-1. (D) BALF cytokines: GM-CSF. (E–J) BALF cytokines: IL-1α, IL-1β, IL-10, IL-17A, IL-27, IL-23. ns, no significance. N = 8-10.
Fig 3: The weak effect of peramivir on chemokines and IL -10 in the serum of mice. (A–C) serum chemokines: CXCL1, CCL5, CXCL10. (D) serum cytokines: IL-10. ns, no significance. N = 10.
Fig 4: Collagens and elastin modulate cytotoxicity and inflammation-associated signaling pathways in NK cells.(A) Gene set enrichment analysis (GSEA) enrichment plots of PI3K-AKT-mTOR, TNFa-NF?B, IL-6–JAK–STAT3, and IL-2–STAT5 signaling in CD49b+ cNK cells in the donor skin compared with the circulation. The enrichment scores (ES) and P values are indicated in each plot. (B) Quantification of phospho-NF?B (pNF?B) (p65) in splenic cNK cells at 30 and 60 min after coculture with m157-MEFs in the presence of different ECM proteins. n = 4 per group, data representative of two independent experiments. (C to G) Quantification of phospho-PLC?1+ (pPLC?1+) (C), pERK1/2+ (D), pNF?B (p65) + (E), pSTAT3+ (F), and pSTAT5+ (G) in splenic cNK cells at 2 and 5 min after stimulation with H2O2 in the presence of different ECM proteins. n = 8 per group from two independent experiments. Representative flow cytometry histograms comparing the phosphorylation of key signaling proteins at 2 and 5 min after stimulation with H2O2 in response to no ECM (gray), collagen I (green), collagen III (orange), and elastin (purple). Black dotted line corresponds to the gating on the basis of the “no ECM – 0 min” histogram for each signaling protein. (H and I) Comparison of pERK1/2 (H) and pNF?B (p65) (I) in splenic NK cells from WT and Lair1-/- mice in response to 2-min H2O2 stimulation in the presence of collagen I. Percentages are normalized on the basis of the no ECM group in WT and Lair1-/- experiments. n = 4 per group; data are representative of two independent experiments. (B to I) Graphs show means ± SD. Mann-Whitney U test; *P < 0.05, **P < 0.01, and ***P < 0.001. (C to G) Each time point is compared with the corresponding time point in no ECM group.
Fig 5: Fully cationic PAMAMs at 40 mg/kg elicit an acute inflammatory responseThis acute inflammatory response to treatment with fully cationic PAMAMs at 40 mg/kg is demonstrated by decreased lymphocyte percentage (A) and increased granulocyte percentage (B) in blood, and elevation of the inflammatory cytokine IP-10 (C) in serum. No such response is seen with mixed surface scavenger treatments. Scavengers were administered to C57BL/6J mice by intraperitoneal injection on days 0, 3, 6, and 9, with sacrifice on day 10 with blood collection for complete blood counts and for serum.Ordinary one-way ANOVAs followed by Tukey’s multiple comparisons tests were run for each of the markers; for panels A and B, comparisons between generation-matched fully cationic and mixed surface scavengers, and between G2 40 mg/kg to saline, are specified. Significance: ∗∗ represents p = 0.0017, ∗∗∗ represents p = 0.0009 and ∗∗∗∗ represents p ≤ 0.0001.
Supplier Page from BioLegend for LEGENDplex™ MU Anti-Virus Response Panel (13-plex) w/ VbP