Fig 1: Colonic lamina propria (LP) cells isolated from control and antibiotic-treated WT and Casp1 KO mice and stained with (A) CD45 (Leukocytes); (B) Ly6G (neutrophils); (C) CD3 (CD3+ T cells); (D) CD4 (CD4+ T cells); (E) CD11c (dendritic cells); and (F) F4/80 (macrophages). Bars represent the percentage of the indicated cell population. Representative figure of two individual experiments. Data are mean (SEM). n = 4–5/group. *: p < 0.05.
Fig 2: Macrophage phenotyping in peritoneal tissue. Representative flow cytometry histograms in peritoneal tissue from control and TUG-891-treated apoE-knockout mice. F4/80 and CD11b+ (A), F4/80, iNOS; CD11b+; F4/80 (B), CD206+; CD11b+; F4/80 (C). Adjacent graphs represent mean ± SEM values, (* p < 0.05; n = 10–14 per group).
Fig 3: Macrophage phenotyping in atherosclerotic plaque. Validation of macrophages morphometry by RT-PCR analysis confirmed a trend toward reduction of M1 markers and no significant increase in M2 genes in the aorta of GW9508-treated apoE−/− mice, (A) (* p < 0.05; ** p < 0.005; n = 6–8 per group). Representative micrographs showing immunohistochemical staining of aortic roots from control and TUG-891-treated apoE-knockout mice. F4/80 (green), nitric oxide synthase 2 (iNOS)/arginase 1 (red) and 4′,6-diamidino-2-phenylindole (DAPI) (blue), confirming the respective macrophage phenotype (white arrows). Adjacent graphs represent mean ± SEM values, (B) (* p < 0.05; n = 5–7 per group).
Fig 4: Representative RT-qPCR expression of genes associated with (A) inflammasome (Pycard, Aim2, Nlrp3, Nlrc4, Nlrp6, Il-1β and Il-18); (B) toll-like receptors (TLR2, -4, -5 and -7); antimicrobial peptides (AMPs-Rentlβ and Reg3γ), the mucus layer component Muc2 and (C) macrophage M1/M2 signature (F4/80, Fitz1, Arg1, Il-6 and Il-12β), the colon of WT and Casp1 KO antibiotic-treated groups. Data are mean (SEM). n= 7–9/group. *: p < 0.05, **: p <0.001. Dashed line indicates a background value of 1 of WT and Casp1 KO-control groups. Abx: Antibiotic.
Fig 5: IGF2BP3 promotes tumor progression and facilitates macrophage infiltration and polarization in mouse HCC model.Igf2bp3_wt and Igf2bp3_ko cells were subcutaneously injected in 6-week-old, male C57BL/6J mice. (A) Tumor volume was measured and recorded every 3 days from initial injection to tumor harvest. (B) Image of the harvested tumors (left), mice were sacrificed on day 21, tumor weight was recorded (right). (C) Kaplan–Meier survival curves of mice bearing Igf2bp3_wt and Igf2bp3_ko tumors. Log-rank tests were used to assess between-group differences in survival. (D) Percentages of CD3+, CD4+, CD8+, CD11b+, F4/80+, F4/80+MHCII+, F4/80+CD206+, CD19+, NK1.1+ and CD11b+Gr-1+ cells in Igf2bp3_wt and Igf2bp3_ko tumors. (E) Images of CD206 immunofluorescence staining for tissue sections of Igf2bp3_wt and Igf2bp3_ko tumors (left) and quantified as mean fluorescence intensity per high power field (right). Scale bar=100 µm. Data are mean±SD. *p<0.05, **p<0.01, ***p<0.001. HCC, hepatocellular carcinoma.
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