EMBO/SourceData huggingface dataset:
Figure 8A-D Growth curves of ΔgdhA, ΔgdhAΔpat and ΔgdhAΔcobB Salmonella strains were measured in minimal medium with 100 mM ammonium and 50 mM glucose in the absence (A) and presence (B) of 20 mM glutamine in the media. in these strains were also measured at different growth stages.E Growth curves of Salmonella ΔgdhA strain complemented with GDH (blue), with GDHK128Q (brown), with GDHK128R (red), with GDHK128R supplemented with 50 mM glutamate in culture media (green), with GDHK128R induced with 1 mM IPTG (purple), with GDHDead (orange) and with GDHK128R induced with 1 mM IPTG (black) in the minimal medium with 50 mM glucose and 100 mM ammonium were compared. Growth curves of total protein levels were normalized by Coomassie Brilliant Blue (CBB) staining. Induction and acetylation of GDH was monitored by western blot. Immunoblots represent at least two independent experimentsG-H Wild-type, ΔcobB and Δpat Salmonella strains were grown under minimal media supplemented with different ratios of glucose and ammonium as indicated. The specific activities of GDH in the cell lysate and steady-state growth rates were determined for each bacterium. Relative GDH activities were normalized to total protein (G) or GDH mRNA (H). Each symbol represents an independent biological replicates
Figure 9A-B Growth curves of Salmonella glnA::glnAWT, glnA::glnAY398S, glnA::glnAY398F, glnA::glnA2KQY398F, glnA::glnA2KQY398S, glnA::glnA2KQY398S-gdhA::gdhAK128Q, and glnA::glnA2KQY398S-gdhA::gdhAK128R strains were measured in minimal medium with 100 mM ammonium and either 5 mM (A) or 50 mM glucose (B) in the media. data are pooled from the three independent experimentsE-I The bacterial loads of the faeces (E and F), caecum (G), spleen (H), and liver (I) of C57BL/6 mouse littermates infected with Salmonella strains glnA::glnAWT (n=4), glnA::glnAY398S (n=4), glnA::glnA2KQY398S (n=4), glnA::glnA2KQY398SgdhA::gdhAK128Q (n=4), and glnA::glnA2KQY398S-gdhA::gdhAK128R (n=4) were measured by counting colony-forming units (CFU) in cultures of serially diluted homogenates of organs on MacConkey agar plates. Each symbol represents an independent biological replicates (E-I)
Figure 7(A) Phenotype of plants complemented with WT DDL or DDL12E1. Four-week-old plants of two independent transgenic lines of pDDL::DDL-FLAG (W7 and W18) or pDDL::DDL12E1-FLAG(E11 and E15) were photographed. Bar=1cm.(A) Phenotype of plants complemented with WT DDL or DDL12E1. Four-week-old plants of two independent transgenic lines of pDDL::DDL-FLAG (W7 and W18) or pDDL::DDL12E1-FLAG(E11 and E15). The expression of transgene was determined by an α-FLAGimmunoblot (bottom).(B) Susceptibility of complementation lines to Pst DC3000 infections. Four-week-old transgenic plants were inoculated with Pst DC3000 (OD600=5x10-4) and the bacterial number was determined at 0 and 3 dpi.(C) PR1 and PR5 induction in transgenic lines. Leaves of four-week-old plants were inoculated with Pst DC3000 (OD600=0.01), and collected at 0, and 24 hpi for qRT-PCR analysis. The data in B and C are shown as mean ± SD (n=3) from three independent repeats with one-way ANOVA analysis and Tukey test (p<0.05). Different letters indicate significant differences.(D) flg22-induced callose deposition in transgenic lines. Leaves of four-week-old plants were inoculated with 500 nM flg22, and callose deposits were stained with aniline blue at 20 hpi. Number of callose deposits was quantified with Image J (mean ± SE, n=10). All experiments were repeated three times with similar results.
Figure 1(C,F) Normalized average fluorescence profiles for mNG-PilG and mNG-PilH of hundreds to thousands of cells The length of each cell is normalized so that the dim pole is positioned at x = -1, the bright pole at x = 1. The fluorescent profile for each cell is normalized to its total fluorescence. Solid lines: mean normalized fluorescence profiles across replicates. Shaded area, standard deviation across replicates.
Figure 2(A) Fluorescence profiles of mNG-PilG in chpA mutants after 2h on surfaces. Solid lines, mean normalized fluorescence profiles across biological replicates. Shaded area, standard deviation across biological replicates.(D) Polar localization profiles of mNG-PilG in ΔfimL and ΔfimL ΔchpA mutant after 2h on surfaces.
Figure 3(A) mNG-PilH fluorescence profiles in chpA mutants after 2h surface growth. To avoid negative effects of low cAMP level on localization of PilH, cpdA was deleted in all displayed strains to rescue cAMP level to WT levels Solid lines, mean normalized fluorescence profiles across biological replicates. Shaded area, standard deviation across biological replicates.
Figure 4C) Fluorescence profiles of mNG-PilHGOF after 2h on surface in chpA mutants. C) Solid lines, mean normalized fluorescence profiles across biological replicates. Shaded area, standard deviation across biological replicates.
Figure 5Displacement maps derived from 50 randomly-selected cell trajectories from three random biological replicates. Each curve corresponds to an individual trajectory. A curve oriented to the top right corresponds to forward twitching, a curve oriented to the top left corresponds to reverse twitching. In each graph, we highlighted three representative tracks for clarity.
Figure 6(A) mNG-PilH fluorescence profiles in ΔpilG after 2h surface growth (low cAMP).(C) mNG-PilH fluorescence profiles in ΔpilG ΔcpdA after 2h surface growth (rescued cAMP).
Figure 7(A) mNG-PilG fluorescence profiles in pilH mutants after 2h surface growth. We included ΔcpdA for comparison since both pilH mutations result in high cAMP levels. PilG is more polar and asymmetric in ΔpilH and pilHLOF. (A Solid lines, mean normalized fluorescence profiles across biological replicates. Shaded area, standard deviation across biological replicates.(D) Time course of PilG localization in pilHGOF on surface. For clarity only the 2h profile of PilG in wild type was included. D) Solid lines, mean normalized fluorescence profiles across biological replicates. Shaded area, standard deviation across biological replicates.
Figure 8(A, Time course fluorescence profiles and polar localization indexes of mNG-PilG in ΔpilA. PilG polar localization index remains unchanged on surfaces in ΔpilA similar to surface-adapted WT(C Time course fluorescence profiles and polar localization indexes of mNG-PilH in ΔpilA. Like in WT, PilH gets recruited to the poles over time in ΔpilA, although at a slower speed
Figure 1A Heatmap of all the DE genes in choroid plexus between the AB and SPF mice. The color scale of the heatmap represents the scaled log2 normalized gene expression. Data information: AB, antibiotics-treated; SPF, specific pathogen-free;
Figure 2A Representative images of immunostainings for ZO-1, OCLN, CDH1 and CLDN1 in choroid plexus of SPF, AB, ABR, GF and GFR mice. Scale bar: 50 μm. B-D Quantification of continuous length (B), maximal length (C), and expressed area (D) of the TJ immunostainings displayed in (A) (n=5, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. AB, antibiotics-treated; ABR, recolonized AB; GF, germ-free; GFR, recolonized GF; SPF, specific pathogen-free; TJ, tight junction.E Representative western blot showing the IgG levels in CSF of SPF, AB, ABR, GF and GFR mice. F Quantitative analysis of IgG in CSF via western blot in (E) (n=4-6, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. AB, antibiotics-treated; ABR, recolonized AB; CSF, cerebrospinal fluid; GF, germ-free; GFR, recolonized GF; SPF, specific pathogen-freeG Assessment of the blood-CSF barrier permeability to 4 kDa FITC-dextran (n=5-9, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. AB, antibiotics-treated; ABR, recolonized AB; CSF, cerebrospinal fluid; GF, germ-free; GFR, recolonized GF; SPF, specific pathogen-free
Figure 3C, D Relative abundance of propionic acid (C) and butyric acid (D) in mice fecal samples (n=4-9, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. **p < 0.01. AB, antibiotics-treated; SPF, specific pathogen-free.
Figure 4B,C TEER (B) and assessment of the 70 kDa FITC-dextran paracellular permeability (C) of primary CPE cells treated as showed in (A) (n=3, technical duplicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. CPE, choroid plexus epithelial; LPS, lipopolysaccharides; TEER, trans-epithelial electrical resistanceD Representative images of immunostainings for ZO-1 and OCLN in primary CPE cells following treatment for 6 h with 1 μM sodium propionate or 1 μM sodium butyrate, with 100 ng/ml LPS stimulation. Scale bar: 50 μm. E The percentage of cells with intact the TJ immunostainings in displayed (D) (n=3, technical duplicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. CPE, choroid plexus epithelial LPS, lipopolysaccharides TJ, tight junction.G Representative images of immunostainings for ZO-1 and OCLN in choroid plexus of sodium propionate or sodium butyrate-treated mice. Scale bar: 50 μm. H-J Quantification of continuous length (H), maximal length (I), and expressed area (J) of TJ immunostainings in (G) (n=5, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. TJ, tight junction.L Representative western blot showing the IgG levels in CSF of sodium propionate or sodium butyrate-treated mice with disrupted gut microbiota via antibiotics treatment. Data information: CSF, cerebrospinal fluid
Figure 5A Representative images of immunostainings for OCLN, CDH1 and ZO-1 in choroid plexus of sham and vagotomized mice. Scale bar: 50 μm. B-D Quantification of continuous length (B), maximal length (C), and expressed area (D) of TJ immunostainings in (A) (n=4, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons *p < 0.05, **p < 0.01, ***p < 0.001. TJ, tight junction.H Representative images of immunostainings for OCLN, CDH1 and ZO-1 in choroid plexus of sodium propionate or sodium butyrate-treated vagotomized mice. Scale bar: 50 μm. I-K Quantification of continuous length (I), maximal length (J), and expressed area (K) of the TJ immunostainings displayed in (H) (n=4, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons *p < 0.05, **p < 0.01, ***p < 0.001. TJ, tight junction.
Figure 6B Representative images of immunostainings for OCLN, CDH1, ZO-1 and CLDN1 in choroid plexus of sodium propionate or sodium butyrate-treated AppNL-G-F mice. Scale bar: 50 μm. C-E Quantification of continuous length (C), maximal length (D), and expressed area (E) of theTJ immunostainings displayed in (B) (n=5-6, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001.I Representative images of 6E10 staining in brain of sodium propionate or sodium butyrate-treated AppNL-G-F mice. Scale bar: 1 mm. J Quantification of Aβ plaque area and number in whole sagittal section of the brain (n=3 mice; one section per mouse). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001.
Figure 7A Representative images of immunostainings for IBA1 and 6E10. Scale bar: 200 μm (up) and 20 μm (down).D Quantification of summarized intersects, ramification index and ending radius by Sholl analysis from immunostained IBA1 signals (n=5-6, biological replicates). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons.*p < 0.05, **p < 0.01.F Plaques were divided into small (< 250 μm2), medium (250-600 μm2), and large (> 600 μm2), and the number of microglia per plaque was quantified (n=5-6 mice; 3-5 plaques per mouse). Data information: Bars represent mean ± SEM. Statistics were performed with one-way ANOVA Bonferroni's post hoc test for multiple comparisons.*p < 0.05, **p < 0.01.
Figure 1(D) Immunocytochemistry of β-catenin in primary WT neurons treated with anti-Shank3 antibody or IgG. Notice the nuclear accumulation of β-catenin upon anti-Shank3 antibody treatment. Arrows point to β-catenin-negative nucleus. Arrowheads point to β-catenin-positive nucleus. : Bar = 50 μm in (D). mice(F) Western-blotting of β-catenin, Axin2 and p-GSK3β(S9) in WT or Shank3-/- primary neurons. mice and 5 batches of cells (F) per group. Mean ratio ± SEM. Two-Tailed unpaired T-test. *P<0.05. **P<0.01. ***P<0.001. WT, wild type. KO, Shank3-/- mice.(G) Western-blotting of SFRP1 and p-β-catenin(S33) in the total proteins, and TCF7L1 in the nuclear protein of WT or Shank3-/- ACC. 3 in mice Mean ratio ± SEM. Two-Tailed unpaired T-test. *P<0.05. **P<0.01. ***P<0.001. WT, wild type. KO, Shank3-/- mice.(H) Western-blotting of Axin2 and p-GSK3β(S9) in the total proteins, and β-catenin(S33) in the nuclear protein of ACC of WT or VPA-treated mice. 3 in H) mice Mean ratio ± SEM. Two-Tailed unpaired T-test. *P<0.05. **P<0.01. ***P<0.001. Con, control.
Figure 2(D) Western-blotting of ADH1, ALDH3 and ENO1 in the ACC of WT and Shank3-/- mice. Notice the up-regulation of ADH1, ALDH3 and ENO1 in Shank3-/- ACC. 3-4 mice in (D) P<0.05. **P<0.01. ***P<0.001. WT, wild type. KO, Shank3-/-.(F) ECAR assay of primary WT and Shank3-/- neurons. Notice the higher ECAR values of Shank3-/- neurons upon glucose and oligomycin stimulation. 5 batches of cells *P<0.05. **P<0.01. ***P<0.001. WT, wild type. KO, Shank3-/(G) LC-MS measurement of lactic acid and pyruvic acid in the ACC of control and VPA-treated mice. Lactic acid is increased in VPA-treated mice. Two-Tailed unpaired T-test. Welch's t-test Pyruvic acid analysis in G *P<0.05. **P<0.01. ***P<0.001. Con, control.
Figure 3(C, D) Spine density and spine subtypes in the ACC of control and β-catenin over-expressing mice. Notice the reduction of total spine density, stubby and mushroom-like spines in β-catenin over-expressing mice. 20 μm in (C Two-Tailed unpaired T-test (Spine analysis excepting mushoom analysis in D. Mann-Whitney U test (Mushroom analysis in D.Patch-clamp recording of mEPSC in the ACC of control and β-catenin over-expressing mice. Both the frequency and average amplitudes of mEPSC were reduced in Wnt over-activated ACC. , 9 neurons from 3 mice in H) Social novelty and social preference scores in , H Amplitude of mEPSC in H.(I) 3-chamber assay of control and β-catenin over-expressing mice. 9-10 mice (I-K) Social novelty and social preference scores in I, Two-tailed paired T-Test (Time in compartment in I).ECAR assay of primary cultured control neurons (GFP+EX3) and β-catenin over-expressing neurons (CaMKII-Cre+EX3). 5 batches of cells ECAR in Max ECAR in M.
Figure 4(A) Typical images of Golgi staining and reconstructed neurons in the ACC of Shank3-/- mice treated with 2-DG (KO+2-DG) or vehicle (KO+Veh). Sholl analysis of pyramidal neurons in the ACC of Shank3-/- mice treated with 2-DG or vehicle. Bar = 50 μm in (A) N = 24-28 neurons from 4 mice in KO, Shank3-/-. Veh, vehicle.(G) Western-blotting of GluR1, PSD95 and Homer1 in the total proteins of Shank3-/- ACC with or without 2-DG treatment. 3 mice in (G) KO, Shank3-/-. Veh, vehicle.resident-intruder assay of Shank3-/- mice treated with 2-DG or vehicle. Notice the improvement of social preference and social interaction by 2-DG treatment. 10-12 mice in KO, Shank3-/-. Veh, vehicle.
Figure 5(A) ECAR assay of primary Shank3-/- neurons treated with or without XAV939. Notice the lower levels of glycolysis in XAV939 treated cells. (B) ECAR assay of primary Shank3-/- neurons treated with or without ICG-001. N = 4-5 batches of cells in Two-Tailed unpaired t-test *P<0.05. **P<0.01. KO, Shank3-/-.(E) Double-immunostaining of ENO1/Axin2 in WT neurons, Shank3-/- neurons, and XAV939 treated Shank3-/- neurons. Notice the colocalization of Axin2/ENO1-immunoreactivity in Shank3-/- neurons and the membrane localization of Axin2-immunoreactivity in XAV939 treated Shank3-/- neurons. Arrows point to membrane Axin2-immunoreactivity. Bar = 5 μm in E. WT, wild type. KO, Shank3-/-.(G) Protein CO-IP of Axin2/ENO1 in WT and Shank3-/- neurons treated with or without XAV939. Notice the strong interaction of Axin2/ENO1 in Shank3-/- neurons and diminished interaction upon XAV939 treatment. per group and 3 samples from 9 mice per group in One-way ANOVA with Tukey's multiple-comparison test WT, wild type. KO, Shank3-/-.
Figure 6Spine length, spine density and spine subtypes of Shank3-/- ACC neurons treated with or without XAV939. Notice the increase of total spine density, stubby and mushroom-like spines and the decrease of average spine length in XAV939 treated Shank3-/- mice. 32 spines from 3 mice in Filopodia analysis in F. Spines analysis excepting filopodia analysis in F. KO, Shank3-/-.(H) Western-blotting of p-PSD95 and Homer1 in WT and Shank3-/- ACC treated with or without XAV939. 4-6 mice in One-way ANOVA with Tukey's multiple-comparison test WT, wild type. KO, Shank3-/-.(I, J) Western-blotting of GluR1 in the total and membrane protein of WT and Shank3-/- neurons treated with or without XAV939. Notice the rescuing effects of XAV939 on the expression of GluR1 in Shank3-/- neurons. 4-6 mice in and 3 samples from 12 mice in (J) per group. One-way ANOVA with Tukey's multiple-comparison test WT, wild type. KO, Shank3-/-.
Figure 7Calcium response of WT and Shank3-/- neurons treated with or without XAV939. Notice that XAV939 treatment significantly restored the amplitude, rising and decay time of calcium response in Shank3-/- neurons. Bar = 15 μm in (A) and 30 μm in magnified images of (A). N = 39 neurons from 3 batches of cells in Kruskal-Wallis H test with Dunn's multiple-comparison test KO, Shank3-/-. Veh, vehicle.Calcium response of WT and Shank3-/- neurons treated with or without XAV939. Notice that XAV939 treatment significantly restored the amplitude, rising and decay time of calcium response in Shank3-/- neurons. N = 39 neurons from 3 batches of cells in Dunn's multiple-comparison test KO, Shank3-/-. Veh, vehicle.(D) Patch-clamp recording of mEPSCs in Shank3-/- ACC treated with or without XAV939. Both the frequency and amplitude of Shank3-/- neurons were increased by XAV939. , 7-8 neurons from 3 mice in (D) KO, Shank3-/-. Veh, vehicle.resident-intruder assays of Shank3-/- mice treated with or without XAV939. Notice the improvement of social preference, social novelty and social interaction of Shank3-/- mice by XAV939 treatment. 8-10 mice KO, Shank3-/-. Veh, vehicle.
Figure 8(B) Western-blotting of β-catenin, p-β-catenin(S33), GSK-3β, p-GSK-3β(S9) and TCF7L1 in neurons derived from WT or Shank3 mutant human ESCs. Notice the similar change of Wnt signaling components as in Shank3-/- mice. N = 3-4 batches of cells in Mean ratio ± SEM. Two-tailed unpaired t-test (Wnt components expression excepting TCF7L1 and GSK3β in Mann-Whitney U test (TCF7L1 expression in B). Welch's t-test (GSK3β expression in B). WT, wild type. KO, Shank3-(C) Protein CO-IP assay of Axin2/ENO1 in WT and Shank3 mutant human NPCs. (D) Protein CO-IP assay of Axin2/ENO1 in WT and Shank3 mutant human neurons. Notice the strong interaction of Axin2/ENO1 Shank3 mutant human neurons. N = 3-4 batches of cells in WT, wild type. KO, Shank3-/ NPC, neural progenitor cell.  (H) ECAR assay of naive human neurons, VPA-pretreated human neurons with or without XAV939 treatment. Notice the higher levels of glycolysis in VPA-pretreated human neurons and the inhibitory effects of XAV939. , 4-5 batches of cells in per group.
Figure 1E Representative mIHC of immune components in CC tumors and adjacent normal tissues. T cells: CD3 (red), B cells: CD20 (green), macrophages: CD68 (pink), NK cells: CD56 (yellow), epithelial cells: Pan-CK (orange). Scale bar =100 μm.H Heatmap showing the expression of marker genes in each subtype of epithelial cells. SCC, squamous cell carcinoma; SCJ, squamocolumnar junction; Imm, immune-related genes; Prolif, hyperproliferation; Colu, columnar epithelium; EMT, epithelial-mesenchymal transition;J Comparison of Overall survival (OS) rates for the high-correlation and low-correlation groups, stratified using the EP0_MUC5B (left panel) and EP2_POSTN (right panel) signatures in TCGA. P values are calculated using the log-rank test (N=255).
Figure 2B Boxplots showing the cell-type proportions of T/NK cells for matched tumor and normal samples (n=5). The scCODA model and the ALDEx2 model were used to examine the differences in T/NK cells' composition. Red bars indicate credible and significant results of scCODA. Stars indicate the significance calculated by ALDEx2 model (* P < 0.05, ** P < 0.01).I Violin plots showing the differentially expressed genes between large and small clone (color-coded as in Fig 2H);
Figure 3H Violin plots showing the association of different B-cell signatures with the response (R, N=15) and no response (NR, N=42) to Pembrolizumab in the Kim cohort. p values calculated using the student's t-test;I Representative mIHC of plasma cells in CC tumor area. plasma cells: CD38+Pan-CK-, scale bar = 100 μm;
Figure 4A, B B cell subsets localization in CC tissues are exhibited by mIHC via differential markers as follow: total B cell: CD20+, GCB: CD20+BCL6-, PC: CD20-CD38+; with scale =500 μm for A, scale = 200 μm for B;C Quantification of B-cell density in Pan-CK+ tumor area, adjacent stroma, and TLS. * P < 0.05, two-way ANOVA following Tukey post-hoc test;E Representative mIHC of CC tumor with CD4+PD-1+CXCL13+ Tfh cells located in TLS (yellow arrows). scale bars =100 μm for left panel, scale bars = 20 μm for right panel;
Figure 5B Boxplots showing the cell-type proportions of myeloid cells for matched tumor and normal samples (n=5). The scCODA model and the ALDEx2 model were used to examine the differences in myeloid cells' composition. Red bars indicate credible and significant results of scCODA. Stars indicate the significance calculated by ALDEx2 model (* P < 0.05).G Comparison of Overall survival (OS) rates for the high-correlation and low-correlation groups, stratified using the Macro_C1QC (upper panel), and Mast_CPA3 (lower panel) signatures in TCGA (N=255). P values are calculated using the log-rank test.
Figure 6B Boxplots showing the cell-type proportions of fibroblast cells for matched tumor and normal samples (n=5).J Comparison of Overall survival (OS) rates for three clusters identified in I. P values are calculated using the log-rank test (n=255).
Figure 1(E) Weight and survival curves of neutrophil specific Nlrp3A350VneoR Gsdmd-/- mice. n≥18
Figure 3(A,B) MPO staining of liver issue used as a marker for myeloid cells including monocytes in both Nlrp3D301N-MRP8 and Nlrp3A350V-MRP8 mutant (n≥3 mice per genotype, representative images shown, bar indicates 250 μM). H&E staining of liver tissue with histologic scoring of liver inflammation (bar indicates 100 μM, representative images are shown). TUNEL staining of liver tissue (Representative images shown, bar indicates 250 μM). Data information: n≥6 mice per genotype, significance determined by unpaired t test (* p < 0.05; ** p < 0.01; *** p < 0.001), data are expressed as mean +/− SD, dots represent individual biological replicats