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94
ATCC ce 10 9 cfu
Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Difco phase 10 6 cfu
Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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MedChemExpress lox 10 11 cfu
Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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ATCC 9 log cfu ml l rhamnosus atcc 7469 strain
Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Miltenyi Biotec assay kit
Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Miltenyi Biotec stemmacs hsccfu assay cocktail
Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid <t>at</t> <t>100</t> mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid at 100 mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: eBioMedicine

Article Title: A next-generation probiotic strain for gut health: Bacteroides cellulosilyticus LYH2 variant with anti-inflammatory and metabolic advantages

doi: 10.1016/j.ebiom.2026.106232

Figure Lengend Snippet: Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid at 100 mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL). Bacterial strains and 5-ASA were given by oral gavage every other day for 21 days before DSS exposure. Colitis was then induced with 3% DSS for 8 days, during which bacterial treatments were paused while 5-ASA continued. (A) Body weight ratio during the experiment. (B) Final body weight. (C) DAI scores during DSS treatment. (D) Representative images of colons from each group. (E) Colon length. (F) Serum monocyte chemoattractant protein-1 (MCP-1) levels. (G) Serum interleukin-1β (IL-1β) levels. (H) Serum tumour necrosis factor-α (TNF-α) levels. (I) Serum interleukin-10 (IL-10) levels. (J) Representative H&E-stained colon sections. Scale bars = 200 μm, 10× objective. (K) Histological scores of colonic tissues. (L) Representative AB-PAS-stained colon sections. Scale bars = 200 μm, 10× objective. (M) Goblet cell number per crypt. (N) Relative mRNA expression of inflammatory and chemokine-related genes ( Tnf , Il1b , Mcp1 , and Cxcl10 ) in colon. Data are mean ± SEM (n = 7). Statistical significance was evaluated using either one-way ANOVA followed by Dunnett's post-hoc test (when normality and homogeneity of variance were met) or the Kruskal–Wallis test followed by Dunn's post-hoc test with Bonferroni correction (when these assumptions were violated), for comparisons of each group versus the DSS group. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: Effects of B . cellulosilyticus LYH2 and comparator treatments on disease severity, inflammation, and goblet cell number in a DSS-induced colitis mouse model. Six-week-old male C57BL/6J mice were randomly assigned to six groups (n = 7): CON (normal drinking water), DSS (3% DSS in drinking water), Ce (3% DSS and B . cellulosilyticus LYH2 at 1 × 10 9 CFU/mL), JCM (3% DSS and B . cellulosilyticus JCM 15632 at 1 × 10 9 CFU/mL), 5-ASA (3% DSS and 5-aminosalicylic acid at 100 mg/kg), and LR (3% DSS and Lactobacillus reuteri ATCC BAA-2837 at 1 × 10 9 CFU/mL).

Techniques: Staining, Expressing