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s aureus mu50  (ATCC)


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    Structured Review

    ATCC s aureus mu50
    Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and <t>Mu50,</t> AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.
    S Aureus Mu50, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 814 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/s aureus mu50/product/ATCC
    Average 99 stars, based on 814 article reviews
    s aureus mu50 - by Bioz Stars, 2026-03
    99/100 stars

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    1) Product Images from "Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903"

    Article Title: Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903

    Journal: JID Innovations

    doi: 10.1016/j.xjidi.2025.100436

    Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and Mu50, AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.
    Figure Legend Snippet: Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and Mu50, AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.

    Techniques Used: Derivative Assay, Control

    Histological analysis of mouse ear skin after treatment with bacterial strains. ( a ) Representative images: H&E-stained sections of mouse ear skin collected on day 9 after treatment with S. aureus (Mu3, Mu50, AD1–AD4), S. epidermidis (AD-derived strains), or TSB. Bar = 50 μm. ( b ) Epidermal thickness: mean epidermal thickness (μm) ± SEM from H&E-stained sections (n = 6–8 mice per group). ( c ) Dermal cellular infiltration: mean dermal cell infiltration ± SEM from the same histological images (n = 5–8 mice per group). Statistical analysis: Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AD, atopic dermatitis; TSB, tryptic soy broth.
    Figure Legend Snippet: Histological analysis of mouse ear skin after treatment with bacterial strains. ( a ) Representative images: H&E-stained sections of mouse ear skin collected on day 9 after treatment with S. aureus (Mu3, Mu50, AD1–AD4), S. epidermidis (AD-derived strains), or TSB. Bar = 50 μm. ( b ) Epidermal thickness: mean epidermal thickness (μm) ± SEM from H&E-stained sections (n = 6–8 mice per group). ( c ) Dermal cellular infiltration: mean dermal cell infiltration ± SEM from the same histological images (n = 5–8 mice per group). Statistical analysis: Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AD, atopic dermatitis; TSB, tryptic soy broth.

    Techniques Used: Staining, Derivative Assay

    Distribution of virulence genes across S. aureus strains. Virulence gene content of 6 S. aureus strains (Mu3, Mu50, AD1, AD2, AD3, and AD4) was analyzed by microarray and grouped by functional categories. Bars represent the number of genes identified within each category per strain. Categories include adhesion factors, staphylococcal superantigen/enterotoxin-like genes, HLG and leukocidins, enterotoxins, proteases, capsule- and biofilm-associated genes, hemolysins, HLb-converting phages, defensin resistance, toxic shock toxin, ACME locus, and other factors. The plot illustrates variation in virulence gene repertoire between strains, with adhesion factors and enterotoxin-like genes showing the highest representation. ACME, arginine catabolic mobile element; HLG, hemolysin .
    Figure Legend Snippet: Distribution of virulence genes across S. aureus strains. Virulence gene content of 6 S. aureus strains (Mu3, Mu50, AD1, AD2, AD3, and AD4) was analyzed by microarray and grouped by functional categories. Bars represent the number of genes identified within each category per strain. Categories include adhesion factors, staphylococcal superantigen/enterotoxin-like genes, HLG and leukocidins, enterotoxins, proteases, capsule- and biofilm-associated genes, hemolysins, HLb-converting phages, defensin resistance, toxic shock toxin, ACME locus, and other factors. The plot illustrates variation in virulence gene repertoire between strains, with adhesion factors and enterotoxin-like genes showing the highest representation. ACME, arginine catabolic mobile element; HLG, hemolysin .

    Techniques Used: Microarray, Functional Assay

    Comparative genomic presence of virulence- and regulation-associated gene families in S. aureus Strains. Heatmaps depict the distribution of gene families associated with ( a ) regulation, ( b ) superantigen-like proteins, ( c ) adhesion, ( d ) biofilm formation, ( e ) leukocidins, ( f ) unconventional virulence factors, and ( g ) proteases across 7 S. aureus strains (MRSA USA300, Mu3, Mu50, AD1, AD2, AD3, and AD 4). Each cell represents the status of a gene in a given strain: presence (yellow), absence (purple), or ambiguous (gray). MRSA, Methicillin-Resistant Staphylococcus aureus .
    Figure Legend Snippet: Comparative genomic presence of virulence- and regulation-associated gene families in S. aureus Strains. Heatmaps depict the distribution of gene families associated with ( a ) regulation, ( b ) superantigen-like proteins, ( c ) adhesion, ( d ) biofilm formation, ( e ) leukocidins, ( f ) unconventional virulence factors, and ( g ) proteases across 7 S. aureus strains (MRSA USA300, Mu3, Mu50, AD1, AD2, AD3, and AD 4). Each cell represents the status of a gene in a given strain: presence (yellow), absence (purple), or ambiguous (gray). MRSA, Methicillin-Resistant Staphylococcus aureus .

    Techniques Used:



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    Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and <t>Mu50,</t> AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.
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    Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and <t>Mu50,</t> AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.
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    Image Search Results


    Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and Mu50, AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.

    Journal: JID Innovations

    Article Title: Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903

    doi: 10.1016/j.xjidi.2025.100436

    Figure Lengend Snippet: Strain-dependent ear swelling responses of clinical isolates upon topical application. ( a ) Experimental protocol: nonclinical S. aureus strains Mu3 and Mu50, AD patient–derived S. aureus and S. epidermidis strains (AD1–AD4), and TSB as a control vehicle were topically applied to the ears of C57BL/6 mice on days 0, 2, 4, 6, and 8. Clinical skin inflammation was assessed by measuring ear thickness. ( b ) Ear swelling over time: mean ear thickness (μm) from day 0 (denoted as D0) to day 9 (denoted as D9) for each treatment group (n = 6–8 mice per group). ( c ) Cumulative ear swelling: individual values and group mean ± SEM for the AUC of ear thickness measurements from D0 to D9 (n = 6–8 mice per group). Statistical analysis: 1-way ANOVA followed by Tukey’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AUC, area under the curve; TSB, tryptic soy broth.

    Article Snippet: Two nonclinical reference strains— S. aureus Mu3 (ATCC 700698) and S. aureus Mu50 (ATCC 700699)—were included in the study.

    Techniques: Derivative Assay, Control

    Histological analysis of mouse ear skin after treatment with bacterial strains. ( a ) Representative images: H&E-stained sections of mouse ear skin collected on day 9 after treatment with S. aureus (Mu3, Mu50, AD1–AD4), S. epidermidis (AD-derived strains), or TSB. Bar = 50 μm. ( b ) Epidermal thickness: mean epidermal thickness (μm) ± SEM from H&E-stained sections (n = 6–8 mice per group). ( c ) Dermal cellular infiltration: mean dermal cell infiltration ± SEM from the same histological images (n = 5–8 mice per group). Statistical analysis: Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AD, atopic dermatitis; TSB, tryptic soy broth.

    Journal: JID Innovations

    Article Title: Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903

    doi: 10.1016/j.xjidi.2025.100436

    Figure Lengend Snippet: Histological analysis of mouse ear skin after treatment with bacterial strains. ( a ) Representative images: H&E-stained sections of mouse ear skin collected on day 9 after treatment with S. aureus (Mu3, Mu50, AD1–AD4), S. epidermidis (AD-derived strains), or TSB. Bar = 50 μm. ( b ) Epidermal thickness: mean epidermal thickness (μm) ± SEM from H&E-stained sections (n = 6–8 mice per group). ( c ) Dermal cellular infiltration: mean dermal cell infiltration ± SEM from the same histological images (n = 5–8 mice per group). Statistical analysis: Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. Symbols indicate statistical significance compared with the following groups: § vehicle, $ S. aureus Mu3, + S. aureus Mu50, @ S. aureus AD3, ∗ S. epidermidis AD3, and ° S. epidermidis AD4. AD, atopic dermatitis; TSB, tryptic soy broth.

    Article Snippet: Two nonclinical reference strains— S. aureus Mu3 (ATCC 700698) and S. aureus Mu50 (ATCC 700699)—were included in the study.

    Techniques: Staining, Derivative Assay

    Distribution of virulence genes across S. aureus strains. Virulence gene content of 6 S. aureus strains (Mu3, Mu50, AD1, AD2, AD3, and AD4) was analyzed by microarray and grouped by functional categories. Bars represent the number of genes identified within each category per strain. Categories include adhesion factors, staphylococcal superantigen/enterotoxin-like genes, HLG and leukocidins, enterotoxins, proteases, capsule- and biofilm-associated genes, hemolysins, HLb-converting phages, defensin resistance, toxic shock toxin, ACME locus, and other factors. The plot illustrates variation in virulence gene repertoire between strains, with adhesion factors and enterotoxin-like genes showing the highest representation. ACME, arginine catabolic mobile element; HLG, hemolysin .

    Journal: JID Innovations

    Article Title: Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903

    doi: 10.1016/j.xjidi.2025.100436

    Figure Lengend Snippet: Distribution of virulence genes across S. aureus strains. Virulence gene content of 6 S. aureus strains (Mu3, Mu50, AD1, AD2, AD3, and AD4) was analyzed by microarray and grouped by functional categories. Bars represent the number of genes identified within each category per strain. Categories include adhesion factors, staphylococcal superantigen/enterotoxin-like genes, HLG and leukocidins, enterotoxins, proteases, capsule- and biofilm-associated genes, hemolysins, HLb-converting phages, defensin resistance, toxic shock toxin, ACME locus, and other factors. The plot illustrates variation in virulence gene repertoire between strains, with adhesion factors and enterotoxin-like genes showing the highest representation. ACME, arginine catabolic mobile element; HLG, hemolysin .

    Article Snippet: Two nonclinical reference strains— S. aureus Mu3 (ATCC 700698) and S. aureus Mu50 (ATCC 700699)—were included in the study.

    Techniques: Microarray, Functional Assay

    Comparative genomic presence of virulence- and regulation-associated gene families in S. aureus Strains. Heatmaps depict the distribution of gene families associated with ( a ) regulation, ( b ) superantigen-like proteins, ( c ) adhesion, ( d ) biofilm formation, ( e ) leukocidins, ( f ) unconventional virulence factors, and ( g ) proteases across 7 S. aureus strains (MRSA USA300, Mu3, Mu50, AD1, AD2, AD3, and AD 4). Each cell represents the status of a gene in a given strain: presence (yellow), absence (purple), or ambiguous (gray). MRSA, Methicillin-Resistant Staphylococcus aureus .

    Journal: JID Innovations

    Article Title: Atopic Dermatitis–like mouse model using early inoculation of patient-derived S. aureus together with MC903

    doi: 10.1016/j.xjidi.2025.100436

    Figure Lengend Snippet: Comparative genomic presence of virulence- and regulation-associated gene families in S. aureus Strains. Heatmaps depict the distribution of gene families associated with ( a ) regulation, ( b ) superantigen-like proteins, ( c ) adhesion, ( d ) biofilm formation, ( e ) leukocidins, ( f ) unconventional virulence factors, and ( g ) proteases across 7 S. aureus strains (MRSA USA300, Mu3, Mu50, AD1, AD2, AD3, and AD 4). Each cell represents the status of a gene in a given strain: presence (yellow), absence (purple), or ambiguous (gray). MRSA, Methicillin-Resistant Staphylococcus aureus .

    Article Snippet: Two nonclinical reference strains— S. aureus Mu3 (ATCC 700698) and S. aureus Mu50 (ATCC 700699)—were included in the study.

    Techniques: