Journal: Journal of Histochemistry and Cytochemistry

Article Title: Altered T-Cell Balance in Lymphoid Organs of a Mouse Model of Colorectal Cancer

doi: 10.1369/0022155416672418

Figure Lengend Snippet: Decreased levels of IFN-γ+IL-17+ double-positive CD4+ T cells in the intestines of ApcMin/+ mice. (A) Percentages of total CD3+CD4+ T cells, IFN-γ+ single-positive, IL-17+ single-positive, and IFN-γ+IL-17+ double-positive CD4+ T cells from spleen, MLN, PPs, SILP, CoLP, and small intestinal IEL of Apc+/+ and ApcMin/+ mice measured by flow cytometry. (B) Representative flow cytometry plots of the IFN-γ versus IL-17 staining. Cells were gated on lymphocytes (based on forward and side scatter), CD45, and CD4. n=4 mice per group. Representative of two independent experiments. **p≤0.01. Abbreviations: MLN, mesenteric lymph node; PPs, Peyer’s patches; SILP, small intestinal lamina propria; CoLP, colonic lamina propria; IEL, intraepithelial lymphocyte; IFN-γ, interferon gamma; Apc, adenomatous polyposis coli; IL-17, interleukin 17.

Article Snippet: Small intestinal and colonic tissue was collected and cells isolated using the Miltenyi Biotec Mouse Lamina Propria Dissociation Kit (Miltenyi Biotec, Auburn, CA) following the manufacturer’s protocol.

Techniques: Flow Cytometry, Staining

Journal: Journal of Histochemistry and Cytochemistry

Article Title: Altered T-Cell Balance in Lymphoid Organs of a Mouse Model of Colorectal Cancer

doi: 10.1369/0022155416672418

Figure Lengend Snippet: Decreased levels of splenic and small intestinal CD8+ cells and decreased CD8+IFN-γ+GnzmB+ cells in PPs in ApcMin/+ mice. (A) Percentages of total CD3+CD8+ T cells, IFN-γ+ single-positive, GnzmB+ single-positive, and IFN-γ+GnzmB+ double-positive CD8+ T cells from spleen, MLN, PPs, SILP, CoLP, and IEL of Apc+/+ and ApcMin/+ mice measured by flow cytometry. (B) CD8 immunofluorescent staining of paraformaldehyde/sucrose–fixed splenic tissue from Apc+/+ and ApcMin/+ mice. Scale bar = 100 µm. n=4 mice per group. Representative of two independent experiments. *p≤0.05, **p≤0.01. Abbreviations: IFN-γ, interferon gamma; GnzmB, granzyme B; Apc, adenomatous polyposis coli; MLN, mesenteric lymph node; PPs, Peyer’s patches; SILP, small intestinal lamina propria; CoLP, colonic lamina propria; IEL, intraepithelial lymphocyte.

Article Snippet: Small intestinal and colonic tissue was collected and cells isolated using the Miltenyi Biotec Mouse Lamina Propria Dissociation Kit (Miltenyi Biotec, Auburn, CA) following the manufacturer’s protocol.

Techniques: Flow Cytometry, Staining

Journal: Nature Cancer

Article Title: Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers

doi: 10.1038/s43018-024-00754-9

Figure Lengend Snippet: a , Left, YAP and TAZ proteins mapped on the TEAD3 surface, as a result of structural alignments with the complex structures (PDB codes 5GN0 , 5OAQ ). The TEAD3 surface is shown in gray with the bound myristate in the buried LP drawn in dark gray. Middle/right, TEAD3–IAG933 cocrystal structure. Bound inhibitor is shown as a stick model with its surface in orange. IAG933 binds within the TEAD Ω-loop pocket to prevent coactivator binding by steric hindrance. The main hydrogen bonds and the salt bridge between protein, inhibitor and water are indicated with dotted green lines. b , Coimmunoprecipitation after a 4-h incubation of NCI-H2052 or MSTO-211H cells with DMSO (0 or –) or the indicated concentrations of IAG933 shows compound-induced inhibition of YAP and TAZ binding to TEAD isoforms. The blots are representative of two individual experiments; IP, immunoprecipitation. c , Dose-dependent inhibition of TEAD target gene expression in MSTO-211H and NCI-H226 cells treated for 24 h with IAG933. IC 50 values are between 11 and 26 nM. d , TEAD target gene inhibition kinetics (mean ± s.e.m., n = 4 of the three genes combined) in four mesothelioma cell lines treated with 300 nM IAG933. e , Antiproliferative activity of IAG933 (72-h treatment) in a panel of mesothelioma, Hippo-altered, non-Hippo-mutated or insensitive cell lines. The GI 50 in MSTO-211H cells was 73 nM. The results from one experiment or the mean of two experiments is shown; amp, amplification; Ex, exon; LoF, loss of function; WT, wild type. f , Real-time live-cell assessments of MSTO-211H and NCI-H226 cells treated with IAG933 or VT104; data show the mean of n = 2 replicates. g , Dose-dependent rescue of YTP activity in a CRISPR knock-in TEAD1 V406A/E408A -mutant YTP-resistant clone of (YAP-amplified) SF-268 glioma cells. These TEAD1 residues correspond to V415 and E417 of the TEAD3 protein. Two-tailed paired t -test P values are included in the graph. h , Correlation of pharmacological and genetic sensitivity profiles in 103 cancer cell lines. Each bar represents one cell line. The y axis shows cell survival values of averaged shRNA drop-out profiles for YAP, TAZ (WWTR1) and TEAD1. Bar colors stratify GI 50 for IAG933 (blue, maximum survival/refractory; red, minimum survival/sensitive). Data were analyzed by two-tailed Spearman correlation test between shRNA sensitivity and GI 50 ; P < 0.0001. i , In vitro pharmacological sensitivity of 283 cancer cell lines to IAG933 (GI 50 versus maximal response ( A max )). Color stratifies geometric mean expression of TEAD target genes CCN1 , CCN2 , ANKRD1 and AMOTL2 . Data were analyzed by two-tailed Spearman correlation test between gene signature and A max ( P < 0.0001) or between gene signature and GI 50 ( P < 0.0001).

Article Snippet: The following Taqman assays (Thermo Fisher Scientific) were used: human CCN1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.3413227.g; human ANKRD1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14671023; human CCN2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14485164.g; human AMOTL2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.39983582; human BCL2L1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.56a.14668121; human MCL1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.26560856; human DUSP6 (6-FAM/ZEN/3′ IBFQ): Hs04329643_s1; human SPYR4 (6-FAM/ZEN/3′ IBFQ): Hs01935412_s1; mouse Ccn1 (6-FAM/ZEN/3′ IBFQ): Mm00487499_g1; mouse Ankrd1 (6-FAM/ZEN/3′ IBFQ): Mm00496512_m1; mouse Gapdh (VIC-MGB): Mm99999915_g1; rat Ankrd1 (6-FAM/ZEN/3′ IBFQ): Rn00566329_m1; rat Ccn2 (6-FAM/ZEN/3′ IBFQ): Rn01537279_g1; rat Actb1 (VIC-MGB): Rn00667869_m1; dog Ccn1 (6-FAM/ZEN/3′ IBFQ): AJX01BF; dog Ankrd1 (6-FAM/ZEN/3′ IBFQ): Cf02662722_m1; dog Ccn2 (6-FAM/ZEN/3′ IBFQ): Cf02641589_m1; dog Gapdh (VIC-MGB): Cf02641589_m1.

Techniques: Binding Assay, Incubation, Inhibition, Immunoprecipitation, Targeted Gene Expression, Activity Assay, Amplification, CRISPR, Knock-In, Mutagenesis, Two Tailed Test, shRNA, In Vitro, Expressing

Journal: Nature Cancer

Article Title: Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers

doi: 10.1038/s43018-024-00754-9

Figure Lengend Snippet: a , Time-dependent effect in quantitative measurements of TEAD target gene expression in cultured mesothelioma cell lines MSTO-211H, NCI-H2052, NCI-H2452, and IST-MES2, with IAG933 PPI inhibitor and VT104 TEAD allosteric inhibitor. Data shown for four replicates, Mean ± SD. Two-tailed paired t test VT-104 [1.2 µM]” vs. “IAG933 [300 nM] using the results from all 3 genes: **p = 0.0002, *** $ , p = 0.0001***, p < 0.0001 for each cell line. b-f , Transcriptional modulation induced byIAG933 in cell lines from non-human species shows a similar range of activity after 24 h treatment. b , human, c , dog, d , rat, e , mouse cell lines were subjected to in vitro treatment with a concentration range of IAG933 for 16 h. mRNA levels of three YAP/TEAD target genes ( CYR61 , ANKRD1 and CTGF ), expressed as relative percentages vs the vehicle control (DMSO), are represented on the y-axis versus tested concentrations of IAG933 (μM) on the log-scaled x-axis. In some cell lines, one of the TEAD target genes could not be detected. f , Lists of the mean IC 50 values (n = 2–4) of IAG933, calculated using Fit models (203) from XLFit (Microsoft). g , Right: characterization of the SF-268 cell clones derived from lentivirus infection with a TEAD1 WT or TEAD1 V406A/E408A mutant. The sensitivity to IAG933 is impaired in the mutant clone. Mean ± SD, results of 6 individual experiments. Left: Rescue experiments that demonstrate TEAD-selectivity of IAG933 and YTPs in a colony formation assay. Cell colonies obtained using CRISPR knock-in engineered clones of the SF-268 YAP-amplified glioma cell line assess the rescue of YTP effects. This cell line mainly expresses and depends on the TEAD1 isoform. Wild-type and TEAD1 V406A/E408A mutant clones were treated with indicated doses of IAG933, YTP-17, or YTP-75. The picture is representative of 3 individual experiments.

Article Snippet: The following Taqman assays (Thermo Fisher Scientific) were used: human CCN1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.3413227.g; human ANKRD1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14671023; human CCN2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14485164.g; human AMOTL2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.39983582; human BCL2L1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.56a.14668121; human MCL1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.26560856; human DUSP6 (6-FAM/ZEN/3′ IBFQ): Hs04329643_s1; human SPYR4 (6-FAM/ZEN/3′ IBFQ): Hs01935412_s1; mouse Ccn1 (6-FAM/ZEN/3′ IBFQ): Mm00487499_g1; mouse Ankrd1 (6-FAM/ZEN/3′ IBFQ): Mm00496512_m1; mouse Gapdh (VIC-MGB): Mm99999915_g1; rat Ankrd1 (6-FAM/ZEN/3′ IBFQ): Rn00566329_m1; rat Ccn2 (6-FAM/ZEN/3′ IBFQ): Rn01537279_g1; rat Actb1 (VIC-MGB): Rn00667869_m1; dog Ccn1 (6-FAM/ZEN/3′ IBFQ): AJX01BF; dog Ankrd1 (6-FAM/ZEN/3′ IBFQ): Cf02662722_m1; dog Ccn2 (6-FAM/ZEN/3′ IBFQ): Cf02641589_m1; dog Gapdh (VIC-MGB): Cf02641589_m1.

Techniques: Targeted Gene Expression, Cell Culture, Two Tailed Test, Activity Assay, In Vitro, Concentration Assay, Control, Clone Assay, Derivative Assay, Infection, Mutagenesis, Colony Assay, CRISPR, Knock-In, Amplification

Journal: Nature Cancer

Article Title: Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers

doi: 10.1038/s43018-024-00754-9

Figure Lengend Snippet: a , Endpoint tumor responses of nine mesothelioma PDX models treated with 240 mg kg −1 YTP-75 once daily for 14–21 days. Data are shown as mean ± s.e.m.; n = 4, 5 or 6 mice per group depending on the model. Data were analyzed by two-tailed unpaired t -test (* P = 0.014, ** P = 0.002, ** # P = 0.0001 and *** P < 0.0001). Gene expression levels and genetic alterations across models retrieved from the Charles River database are displayed on the bottom. b , c , Antitumor efficacy of IAG933 or YTP-75 and change in body weight in two NF2 loss-of-function mouse xenograft models of non-mesothelioma cancers. Data are shown as mean ± s.e.m. and were analyzed by two-tailed paired t -tests (** P = 0.001, * P = 0.0146 and * # P = 0.0397); n = 5 per group (5938-HX triple-negative breast ductal carcinoma PDX model; b ) and n = 6 per group (NCI-H292 lung carcinoma CDX model; c ). d , Dose-dependent inhibition of the CCN2 TEAD target gene by YTP-75 (24-h treatment) in NIH-3T3 cells stably expressing YAP – MAML2 or TAZ – CAMTA1 fusion genes. Calculated IC 50 values are between 82 and 292 nM. e , Dose-dependent antitumor efficacy and change in body weight of IAG933 in subcutaneous NIH-3T3 xenograft tumors expressing TAZ–CAMTA1. Data are shown as mean ± s.e.m. and were analyzed by one-way ANOVA; n = 6 per group; * P = 0.0252.

Article Snippet: The following Taqman assays (Thermo Fisher Scientific) were used: human CCN1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.3413227.g; human ANKRD1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14671023; human CCN2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14485164.g; human AMOTL2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.39983582; human BCL2L1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.56a.14668121; human MCL1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.26560856; human DUSP6 (6-FAM/ZEN/3′ IBFQ): Hs04329643_s1; human SPYR4 (6-FAM/ZEN/3′ IBFQ): Hs01935412_s1; mouse Ccn1 (6-FAM/ZEN/3′ IBFQ): Mm00487499_g1; mouse Ankrd1 (6-FAM/ZEN/3′ IBFQ): Mm00496512_m1; mouse Gapdh (VIC-MGB): Mm99999915_g1; rat Ankrd1 (6-FAM/ZEN/3′ IBFQ): Rn00566329_m1; rat Ccn2 (6-FAM/ZEN/3′ IBFQ): Rn01537279_g1; rat Actb1 (VIC-MGB): Rn00667869_m1; dog Ccn1 (6-FAM/ZEN/3′ IBFQ): AJX01BF; dog Ankrd1 (6-FAM/ZEN/3′ IBFQ): Cf02662722_m1; dog Ccn2 (6-FAM/ZEN/3′ IBFQ): Cf02641589_m1; dog Gapdh (VIC-MGB): Cf02641589_m1.

Techniques: Two Tailed Test, Gene Expression, Inhibition, Stable Transfection, Expressing

Journal: Nature Cancer

Article Title: Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers

doi: 10.1038/s43018-024-00754-9

Figure Lengend Snippet: a , Antiproliferative activity dose matrices, 6-day readout; data represent the mean values of triplicates for IAG933 with dabrafenib, IAG933 with dabrafenib and LTT462 and IAG933 with dabrafenib and trametinib in HT-29 and MDST8 BRAF V600E -mutated CRC cells. b , CCN1 and CCN2 TEAD target gene expression in three cell lines after 24 h of treatment with dabrafenib (Dab) plus trametinib (Tram), YTP-10 or all three. Data are shown as mean ± s.e.m.; n = 4 for DMSO, n = 8 for YTP-10, n = 3 for dabrafenib/trametinib and n = 3 for the combination. Data were analyzed by one-way ANOVA, and comparisons to DMSO are shown (*** P < 0.001; other P values are indicated on graphs). c , Antitumor efficacy of IAG933, dabrafenib + LTT462 or all three therapeutic agents combined in mouse HT-29 xenografts. Data are shown as mean ± s.e.m.; n = 5 per group. Data were analyzed by one-way ANOVA, and comparisons to the vehicle group are shown (* P = 0.0255). 2QD indicates twice daily. d , Antitumor efficacy of dabrafenib + trametinib ± cetuximab or YTP-75 in the 5238-HX mouse PDX model. Data are shown as mean ± s.e.m.; n = 10 for the vehicle group, n = 18 for the dabrafenib/trametinib group, n = 32 for the dabrafenib/trametinib + cetuximab group and n = 6 for the dabrafenib/trametinib + YTP-75 group. Data were analyzed by one-way ANOVA, and triple combinations were compared (* P = 0.083) or body weights were compared to the vehicle group (** P = 0.0471 and *** P < 0.0002).

Article Snippet: The following Taqman assays (Thermo Fisher Scientific) were used: human CCN1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.3413227.g; human ANKRD1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14671023; human CCN2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.14485164.g; human AMOTL2 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.39983582; human BCL2L1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.56a.14668121; human MCL1 (6-FAM/ZEN/3′ IBFQ): Hs.PT.58.26560856; human DUSP6 (6-FAM/ZEN/3′ IBFQ): Hs04329643_s1; human SPYR4 (6-FAM/ZEN/3′ IBFQ): Hs01935412_s1; mouse Ccn1 (6-FAM/ZEN/3′ IBFQ): Mm00487499_g1; mouse Ankrd1 (6-FAM/ZEN/3′ IBFQ): Mm00496512_m1; mouse Gapdh (VIC-MGB): Mm99999915_g1; rat Ankrd1 (6-FAM/ZEN/3′ IBFQ): Rn00566329_m1; rat Ccn2 (6-FAM/ZEN/3′ IBFQ): Rn01537279_g1; rat Actb1 (VIC-MGB): Rn00667869_m1; dog Ccn1 (6-FAM/ZEN/3′ IBFQ): AJX01BF; dog Ankrd1 (6-FAM/ZEN/3′ IBFQ): Cf02662722_m1; dog Ccn2 (6-FAM/ZEN/3′ IBFQ): Cf02641589_m1; dog Gapdh (VIC-MGB): Cf02641589_m1.

Techniques: Activity Assay, Targeted Gene Expression

Journal: Chemmedchem

Article Title: Borcalein: a Carborane‐Based Analogue of Baicalein with 12‐Lipoxygenase‐Independent Toxicity

doi: 10.1002/cmdc.202100588

Figure Lengend Snippet: Selectivity index values of borcalein and baicalein. The selectivity index was calculated as IC 50 MRC‐5/IC 50 tested compound.

Article Snippet: Cultivation of the cells : Human melanoma A375, mouse melanoma B16 and B16F10, human colon cancer HCT116 and SW480, mouse colon cancer CT26CL25 and non‐malignant MRC‐5 cell lines were purchased from American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques:

Journal: Chemmedchem

Article Title: Borcalein: a Carborane‐Based Analogue of Baicalein with 12‐Lipoxygenase‐Independent Toxicity

doi: 10.1002/cmdc.202100588

Figure Lengend Snippet: Mode of cytotoxicity of borcalein in comparison to baicalein. CT26CL25 cells were treated with IC 50 doses of borcalein and baicalein for 48 h and then subjected to: ( A ) CFSE assay, ( B ) annexin/propidium iodide, ( C ) apostat, and ( D ) acridine orange staining. Cells were analysed by flow cytometry, one representative experiment out of three is shown.

Article Snippet: Cultivation of the cells : Human melanoma A375, mouse melanoma B16 and B16F10, human colon cancer HCT116 and SW480, mouse colon cancer CT26CL25 and non‐malignant MRC‐5 cell lines were purchased from American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Comparison, CFSE Assay, Staining, Flow Cytometry

Journal: Microbiology Spectrum

Article Title: An Engineered λ Phage Enables Enhanced and Strain-Specific Killing of Enterohemorrhagic Escherichia coli

doi: 10.1128/spectrum.01271-22

Figure Lengend Snippet: An engineered λ phage with enhanced and strain-specific killing ability against enterohemorrhagic Escherichia coli (EHEC). (a) Overview of the engineering of the lambda (λ) phage. First, an 8-kb fragment on the wild-type λ phage (wtλ) was engineered to contain the cas3 gene, the cascade genes, and a CRISPR array containing a spacer specifically targeting the eae gene of the E. coli EHEC strain; the spacer was repeated six times. In addition, the cro gene was knocked out from the wtλ genome. See Materials and Methods for more details. (b) Antibacterial curves of the wild-type (wtλ) and engineered (Eλ) phages against EHEC in vitro. (c) Killing specificity test of the Eλ against 22 E. coli strains, including 3 EHEC strains, 4 EPEC strains, 5 common laboratory strains, and 10 gut commensal strains isolated from human feces. “Target site+” indicates strains that contain the eae gene and can be targeted by the CRISPR spacer, while “Target site−” indicates strains that either do not contain the eae gene or the sequences of their eae genes do not match the CRISPR spacer. The survival rate was measured at the 12th hour after infection with an MOI (multiplicity of infection) of 10 and calculated as CFU (with Eλ)/CFU (without Eλ). All of the data are expressed as the mean ± SD. ( n = 3; ***, P < 0.001, one-way ANOVA and Tukey’s posttest).

Article Snippet: We further validated the effect of Eλ in vivo using an EHEC (ATCC 35150)-colonized mouse model.

Techniques: CRISPR, In Vitro, Isolation, Infection

Journal: Microbiology Spectrum

Article Title: An Engineered λ Phage Enables Enhanced and Strain-Specific Killing of Enterohemorrhagic Escherichia coli

doi: 10.1128/spectrum.01271-22

Figure Lengend Snippet: Eλ eliminates EHEC in vivo and rescues EHEC-infected mice. (a) Experimental design using an EHEC infection mouse model. Ten mice were used for each of the four groups. (b) Weight changes ( y axis) as a function of time (days, x axis) in the four groups. Weight changes were calculated as percent change from baseline weight on day 0 throughout the experiment. All data are expressed as the mean ± SD. ( n = 10; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; one-way ANOVA and Tukey’s posttest). (c) Mouse survival rate ( y axis) as a function of time (days, x axis) in the four groups. ( n = 10; *, P < 0.05; ****, P < 0.0001; log-rank [Mantel-Cox] test). (d) Total viable EHEC counts (CFU) in 100 mg mouse feces. All data are expressed as mean ± SD ( n = 10; ****, P < 0.0001, one-way ANOVA and Tukey’s posttest).

Article Snippet: We further validated the effect of Eλ in vivo using an EHEC (ATCC 35150)-colonized mouse model.

Techniques: In Vivo, Infection

Journal: Microbiology Spectrum

Article Title: An Engineered λ Phage Enables Enhanced and Strain-Specific Killing of Enterohemorrhagic Escherichia coli

doi: 10.1128/spectrum.01271-22

Figure Lengend Snippet: The Eλ phage alleviated EHEC-induced tissue damage and inflammation markers. (a) Statistical analysis of colon lengths of all mice from the four groups. (b) Representative images of hematoxylin and eosin (H&E)-stained colon; the colon was taken from mice on day 4. Magnification, ×200; scale bars, 100 μm. (c) Histological scores summarizing the tissue damage from the images. Four mice were analyzed from each of the four groups. Each of the three variables, namely, edema, inflammation, and epithelial damage, was scored on a scale of 0 to 4 according to the evaluation criteria published by Selle et al. . (d) Levels of IgA from the serum (left) and feces (right). (e to g) Levels of IL-6 (e), IgG1 (f), and IgG2a (g) from mouse serum. All data are expressed as the mean ± SD ( n = 4; *, P < 0.05; **, P < 0.01; ***, P < 0.001; one-way ANOVA and Tukey’s posttest).

Article Snippet: We further validated the effect of Eλ in vivo using an EHEC (ATCC 35150)-colonized mouse model.

Techniques: Staining

Journal: Microbiology Spectrum

Article Title: An Engineered λ Phage Enables Enhanced and Strain-Specific Killing of Enterohemorrhagic Escherichia coli

doi: 10.1128/spectrum.01271-22

Figure Lengend Snippet: The Eλ phage restored EHEC-induced gut microbiota dysbiosis. (a) Alpha diversity analysis of mouse gut microbiota community compositions of the four experimental groups measured using Shannon (left) and Simpson (right) indexes. ( n = 4; *, P < 0.05; Wilcoxon rank-sum test). (b) Principal-coordinate analysis (PCoA) of the gut microbiota community compositions of the four groups (beta diversity).

Article Snippet: We further validated the effect of Eλ in vivo using an EHEC (ATCC 35150)-colonized mouse model.

Techniques: