Fig 1: SLURP1 promotes the pathogenesis of E coli K1 meningitis in mice model. (A) Survival curve of C57BL/6 mice treated with SLURP1 (100 mg/kg body weight) + E. coli K1 (1 × 106) or treated with only E coli K1 (1 × 106). SLURP1 was intraperitoneally injected 2 days before E coli K1 challenge. n = 10 per group. (B, C) Pathogen (B) and PMN (C) counts in the CSF of E coli K1-infected mice pretreated with BSA or indicated doses of SLURP1. (D) The OD620 values of Evans blue extracted from the brain of E coli K1-infected mice pretreated with BSA or indicated doses of SLURP1. (E) Representative H&E staining of the cortex sections, scale bar = 200 µm; and (F) meningeal inflammation score. (G–I) The cytokines levels in the CSF were analyzed by ELISA: TNF-a (G), MMP-9 (H), and ICAM-1 (I). The H&E staining are representative of two independent experiments (E). Data are presented as mean ± SEM from two independent experiments. Each dot indicates an individual mouse (n = 5). *p < 0.05; **p < 0.01; ***p < 0.001 by log-rank test (A), Student’s t-test (F), and one-way ANOVA followed by Bonferroni post-hoc test (B–D, G–I). ns, not significant.
Fig 2: A20 affects MMP-9 and ZO-1 and maintains the integrity of the BBB after SAH. (A, B) Lentivirus transfection for A20 expression affected the expression of MMP-9 and ZO-1 as revealed by representative western blots. (C) A20 expression affected the activity of MMP-9 as revealed by ELISA. (D) Evaluation of the integrity of the BBB by injection of Evans blue dye. A20 played a role in maintaining the integrity of the BBB after SAH. Data are expressed as mean ± SEM, n = 6, *p < 0.05, **p < 0.01, ***p < 0.005, ns versus SAH. ns, non-significant.
Fig 3: Cardiac fibrosis and apoptosis in mice treated with saline solution (Sham), EMPA 10 mg/kg/day, DOXO 2.17 mg/kg/day or EMPA associated to DOXO (n = 6 for each group). A representative images of the interstitial fibrosis (collagen content, indicative of the fibrosis) in cardiac tissue. B cardiac collagen quantification (% of collagen of area) in heart tissue. C Heart pro-collagen 1-a1 quantification in cardiac tissue (ng/mg of total protein); D MMP-9 content ( pg/mg of protein) in cardiac tissue, indicative of fibrosis. E apoptosis imaging in cardiac tissue ( in green, apoptotic nuclei). F apoptotic nuclei, expressed as relative percentage of positive nuclei in heart tissue (two-way ANOVA with a Bonferroni post hoc test). G Caspase-3 expression in cardiac tissue (expressed as ng of Caspase-3/g of tissue). H SGLT-2 protein expression in cardiac and renal tissues of C57B/6 mice through western blot analysis. I Real Time -PCR analysis indicating the relative mRNA expression of SGLT-2 in cardiac and renal tissues of C57B/6 mice. Values are expressed ± SD. *** P < 0.001; **P < 0.01; * P < 0.05; ns: not significant
Fig 4: FMD does not improve immune-therapy efficacy against lung LLC1 cancer, but reduces immune-therapy related cardiac damage.A Schedule of tumor implantation and treatment for B16F10 syngeneic tumor models. B LLC1 Tumor growth in immunocompetent C57/BL6 syngeneic mice treated with isotype control, anti-OX40/anti-PD-L1 and anti-PD-1/anti–CTLA4 and fed with standard diet or FMD (AL IgG n = 13; FMD IgG n = 13; AL OX40PDL1 n = 12; FMD OX40PDL1 n = 14; AL PD1CTL4 n = 12; FMD PD1CTLA4 n = 13). Analysis of tumor immune infiltrate by FACS: C CD8+ on CD45+ T cells (n = 5); D GZMB+ on CD8+ T cells (n = 5); E CD4+ on CD45+ T cell (n = 5); F FOXP3+ on CD4+ T cells (n = 5); G H&E staining in the heart of C57/J mice bearing LLC1 lung tumor and treated with IgG or anti-OX40/anti-PD-L1 or anti-PD-1/anti-CTLA-4; H CD3 and CD8 staining in the heart of C57/J mice bearing LLC1 lung tumor and treated with IgG or anti-OX40/anti-PD-L1 or anti-PD-1/anti-CTLA-4 (3 tissue sections for each tumor; 5 tumors per each group); I Quantification of heart fibrosis and necrosis in the different experimental group; L Quantification of pro collagen 1α1 and MMP9 in the heart belonging to different experimental group (n = 5); M Quantification of CD3 and CD8 cell count in heart belonging to different experimental group (3 tissue sections for each tumor; 5 tumors per each group). Statistical analysis was performed using one-way analysis of variance (ANOVA) and Global Kruskal Wallis test. P values were determined by One-way ANOVA with Tukey’s post analysis. Differences were considered significant when P < 0.05. All data are represented as mean ± SEM. Source data are provided as a Source Data file.
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