clinical strain ss1 Search Results


95
ATCC strain ss1
Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain <t>SS1</t> following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.
Strain Ss1, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
ATCC helicobacter pylori
FIGURE 2 Representative reactivity of monoclonal antibodies against lysates from different bacterial species and strains. Purified monoclonal antibodies against <t>Helicobacter</t> pylori SOD (clone 1F11), catalase (2E11), or thiol peroxidase (H1.1) (all IgG1 at 100 ng/mL) were incubated with various bacterial lysates that had been subjected to SDS-PAGE and then transferred to nitrocellulose by Western blot. After washing, membranes were incubated with a HRP-conjugated goat anti-mouse IgG secondary antibody, before developing with an ECL™ Western Blotting Detection Kit. Samples 1 and 2 were clinical isolates of H. pylori
Helicobacter Pylori, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC vitro test strains
FIGURE 2 Representative reactivity of monoclonal antibodies against lysates from different bacterial species and strains. Purified monoclonal antibodies against <t>Helicobacter</t> pylori SOD (clone 1F11), catalase (2E11), or thiol peroxidase (H1.1) (all IgG1 at 100 ng/mL) were incubated with various bacterial lysates that had been subjected to SDS-PAGE and then transferred to nitrocellulose by Western blot. After washing, membranes were incubated with a HRP-conjugated goat anti-mouse IgG secondary antibody, before developing with an ECL™ Western Blotting Detection Kit. Samples 1 and 2 were clinical isolates of H. pylori
Vitro Test Strains, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

Journal: Frontiers in Microbiology

Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

doi: 10.3389/fmicb.2025.1750216

Figure Lengend Snippet: Inhibitory and bactericidal effects of NBP and NBP-NPs. (A) The colony morphology of H. pylori strains after treatment with various drug concentrations. (B) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP. (C) Bacterial growth inhibition kinetics of strain ATCC 700392 following treatment with NBP-NPs. (D) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP. (E) Bacterial growth inhibition kinetics of strain SS1 following treatment with NBP-NPs.

Article Snippet: The standard strain ATCC 700392 and the clinical strain SS1 were exposed to NBP and NBP-NPs solutions at concentrations of 2 × MIC, 1 × MIC, and 0.5 × MIC under microaerophilic conditions at 37 °C with shaking at 150 rpm for 3 days.

Techniques: Inhibition

Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

Journal: Frontiers in Microbiology

Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

doi: 10.3389/fmicb.2025.1750216

Figure Lengend Snippet: Molecular mechanisms of drug action against H. pylori . (A) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in ATCC 700392. (B) Impact of NBP and NBP-NPs treatment on virulence gene expression levels in SS1. (C–E) Effect of drug treatment on urease activity in ATCC 700392. (F–H) Effect of drug treatment on urease activity in SS1 ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control group). (I) Drug-induced ultrastructural alterations in H. pylori SS1 observed by SEM (30.0 kx, 40.0 kx, 70.0 kx). CagA protein expression in H. pylori SS1 treated with (J) NBP and (K) NBP-NPs ( n =3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. con trol group).

Article Snippet: The standard strain ATCC 700392 and the clinical strain SS1 were exposed to NBP and NBP-NPs solutions at concentrations of 2 × MIC, 1 × MIC, and 0.5 × MIC under microaerophilic conditions at 37 °C with shaking at 150 rpm for 3 days.

Techniques: Gene Expression, Activity Assay, Control, Expressing

Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

Journal: Frontiers in Microbiology

Article Title: In vitro study on anti- Helicobacter pylori effects of DL-3-n-butylphthalide-loaded silk fibroin nanoparticles

doi: 10.3389/fmicb.2025.1750216

Figure Lengend Snippet: Metabolite analysis of H. pylori SS1 treated in vitro with NBP and its nanoparticles. (A) TIC of QC sample chromatogram. (B) TIC of bacterial metabolites. The vertical axis represents the normalized intensity offset index for each group. The three distinct colors correspond to the three different experimental groups. (C) PCA of bacterial metabolites. (D) PLS-DA of bacterial metabolites. (E) Venn diagram analysis of differential metabolites between the NBP group and the NBP-NPs group. (F) Volcano plot depicting differential metabolites in the NBP group versus the control. (G) Volcano plot depicting differential metabolites in the NBP-NPs group versus the control. Metabolites marked in red, green, and gray represent those that are significantly upregulated, downregulated, or show no significant change, respectively. (H) Clustered heatmap showing the metabolite profiles of the NBP group compared to the control. (I) Clustered heatmap showing the metabolite profiles of the NBP-NPs group compared to the control. The color bar represents the relative abundance level of metabolites, with gradients from blue (low) to red (high). (J) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP. (K) KEGG pathway enrichment analysis of metabolites from H. pylori SS1 after treatment with NBP-NPs. The size of each circle corresponds to the number of metabolites mapped to the pathway, and the color depth reflects the significance of the enrichment.

Article Snippet: The standard strain ATCC 700392 and the clinical strain SS1 were exposed to NBP and NBP-NPs solutions at concentrations of 2 × MIC, 1 × MIC, and 0.5 × MIC under microaerophilic conditions at 37 °C with shaking at 150 rpm for 3 days.

Techniques: In Vitro, Control

FIGURE 2 Representative reactivity of monoclonal antibodies against lysates from different bacterial species and strains. Purified monoclonal antibodies against Helicobacter pylori SOD (clone 1F11), catalase (2E11), or thiol peroxidase (H1.1) (all IgG1 at 100 ng/mL) were incubated with various bacterial lysates that had been subjected to SDS-PAGE and then transferred to nitrocellulose by Western blot. After washing, membranes were incubated with a HRP-conjugated goat anti-mouse IgG secondary antibody, before developing with an ECL™ Western Blotting Detection Kit. Samples 1 and 2 were clinical isolates of H. pylori

Journal: Helicobacter

Article Title: Superoxide dismutase from Helicobacter pylori suppresses the production of pro-inflammatory cytokines during in vivo infection.

doi: 10.1111/hel.12459

Figure Lengend Snippet: FIGURE 2 Representative reactivity of monoclonal antibodies against lysates from different bacterial species and strains. Purified monoclonal antibodies against Helicobacter pylori SOD (clone 1F11), catalase (2E11), or thiol peroxidase (H1.1) (all IgG1 at 100 ng/mL) were incubated with various bacterial lysates that had been subjected to SDS-PAGE and then transferred to nitrocellulose by Western blot. After washing, membranes were incubated with a HRP-conjugated goat anti-mouse IgG secondary antibody, before developing with an ECL™ Western Blotting Detection Kit. Samples 1 and 2 were clinical isolates of H. pylori

Article Snippet: Helicobacter pylori (two clinical isolates and mouse- adapted strain SS1),15 Helicobacter felis (CS1),16 Helicobacter bilis (ATCC 51630),17 and Citrobacter rodentium (ICC169) were grown initially on horse blood agar plates at 37°C under microaerophilic (Helicobacter spp.) or aerobic (C. rodentium) conditions.

Techniques: Bioprocessing, Purification, Incubation, SDS Page, Western Blot

FIGURE 3 Injection of monoclonal antibodies against Helicobacter pylori enzymes into H. pylori-infected mice. Groups of C57BL/6 mice (n = 6/7), infected three months earlier with 107 H. pylori SS1, were injected intraperitoneally with an IgG1 monoclonal antibody (mAb) against either H. pylori superoxide dismutase (HpSOD; clone 1F11, n = 6), catalase (Kat; clone 2E11, n = 6), or thiol peroxidase (Tpx; clone H1.1, n = 6). Infected control mice were treated with isotype control antibody (anti-sheep CD4 IgG1, n = 7). Five days later, samples were collected for analysis. A, Antibody levels in gastric scrapings and sera were determined by ELISA. All three antibodies were specifically detected in the sera and gastric mucosal secretions of mice receiving injections of those antibodies (one-way ANOVA on log-transformed endpoint titers). B, H. pylori colonization levels were quantified by colony-forming assay (CFU, colony-forming units). The antibody treatments had no significant effect on H. pylori colonization (one-way ANOVA on log-transformed CFU)

Journal: Helicobacter

Article Title: Superoxide dismutase from Helicobacter pylori suppresses the production of pro-inflammatory cytokines during in vivo infection.

doi: 10.1111/hel.12459

Figure Lengend Snippet: FIGURE 3 Injection of monoclonal antibodies against Helicobacter pylori enzymes into H. pylori-infected mice. Groups of C57BL/6 mice (n = 6/7), infected three months earlier with 107 H. pylori SS1, were injected intraperitoneally with an IgG1 monoclonal antibody (mAb) against either H. pylori superoxide dismutase (HpSOD; clone 1F11, n = 6), catalase (Kat; clone 2E11, n = 6), or thiol peroxidase (Tpx; clone H1.1, n = 6). Infected control mice were treated with isotype control antibody (anti-sheep CD4 IgG1, n = 7). Five days later, samples were collected for analysis. A, Antibody levels in gastric scrapings and sera were determined by ELISA. All three antibodies were specifically detected in the sera and gastric mucosal secretions of mice receiving injections of those antibodies (one-way ANOVA on log-transformed endpoint titers). B, H. pylori colonization levels were quantified by colony-forming assay (CFU, colony-forming units). The antibody treatments had no significant effect on H. pylori colonization (one-way ANOVA on log-transformed CFU)

Article Snippet: Helicobacter pylori (two clinical isolates and mouse- adapted strain SS1),15 Helicobacter felis (CS1),16 Helicobacter bilis (ATCC 51630),17 and Citrobacter rodentium (ICC169) were grown initially on horse blood agar plates at 37°C under microaerophilic (Helicobacter spp.) or aerobic (C. rodentium) conditions.

Techniques: Injection, Bioprocessing, Infection, Control, Enzyme-linked Immunosorbent Assay, Transformation Assay

FIGURE 4 Gastric cytokine levels in H. pylori-infected mice treated with anti- HpSOD. Groups of C57BL/6 mice (n = 6/7), infected 3 months earlier with 107 H. pylori SS1, were injected intraperitoneally with an IgG1 monoclonal antibody against either H. pylori superoxide dismutase (HpSOD; clone 1F11, n = 6), catalase (Kat; clone 2E11, n = 6), or thiol peroxidase (Tpx; clone H1.1, n = 6). Infected control mice were treated with isotype control antibody (anti- sheep CD4 IgG1, n = 7). Five days later, half stomachs were homogenized and cytokine levels were quantified by ELISA. Stomachs from mice treated with anti-HpSOD had significantly higher levels of TNF-α, IL-6, KC, MIP-2, IFN-γ, and IL-13 compared with those from infected mice receiving isotype controls (*ANOVA). Neither the anticatalase nor antithiol peroxidase monoclonal antibodies had any significant effect on cytokine concentrations

Journal: Helicobacter

Article Title: Superoxide dismutase from Helicobacter pylori suppresses the production of pro-inflammatory cytokines during in vivo infection.

doi: 10.1111/hel.12459

Figure Lengend Snippet: FIGURE 4 Gastric cytokine levels in H. pylori-infected mice treated with anti- HpSOD. Groups of C57BL/6 mice (n = 6/7), infected 3 months earlier with 107 H. pylori SS1, were injected intraperitoneally with an IgG1 monoclonal antibody against either H. pylori superoxide dismutase (HpSOD; clone 1F11, n = 6), catalase (Kat; clone 2E11, n = 6), or thiol peroxidase (Tpx; clone H1.1, n = 6). Infected control mice were treated with isotype control antibody (anti- sheep CD4 IgG1, n = 7). Five days later, half stomachs were homogenized and cytokine levels were quantified by ELISA. Stomachs from mice treated with anti-HpSOD had significantly higher levels of TNF-α, IL-6, KC, MIP-2, IFN-γ, and IL-13 compared with those from infected mice receiving isotype controls (*ANOVA). Neither the anticatalase nor antithiol peroxidase monoclonal antibodies had any significant effect on cytokine concentrations

Article Snippet: Helicobacter pylori (two clinical isolates and mouse- adapted strain SS1),15 Helicobacter felis (CS1),16 Helicobacter bilis (ATCC 51630),17 and Citrobacter rodentium (ICC169) were grown initially on horse blood agar plates at 37°C under microaerophilic (Helicobacter spp.) or aerobic (C. rodentium) conditions.

Techniques: Infection, Injection, Control, Enzyme-linked Immunosorbent Assay, Bioprocessing