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Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916
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| Zeitschriftentitel: | Journal of the European Academy of Dermatology and Venereology |
|---|---|
| Personen und Körperschaften: | , , , , , , |
| In: | Journal of the European Academy of Dermatology and Venereology, 33, 2019, 6, S. 1177-1188 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Hesse‐Macabata, J. Morgner, B. Morgenstern, S. Grimm, M.O. Elsner, P. Hipler, U.C. Wiegand, C. Hesse‐Macabata, J. Morgner, B. Morgenstern, S. Grimm, M.O. Elsner, P. Hipler, U.C. Wiegand, C. |
|---|---|
| author |
Hesse‐Macabata, J. Morgner, B. Morgenstern, S. Grimm, M.O. Elsner, P. Hipler, U.C. Wiegand, C. |
| spellingShingle |
Hesse‐Macabata, J. Morgner, B. Morgenstern, S. Grimm, M.O. Elsner, P. Hipler, U.C. Wiegand, C. Journal of the European Academy of Dermatology and Venereology Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 Infectious Diseases Dermatology |
| author_sort |
hesse‐macabata, j. |
| spelling |
Hesse‐Macabata, J. Morgner, B. Morgenstern, S. Grimm, M.O. Elsner, P. Hipler, U.C. Wiegand, C. 0926-9959 1468-3083 Wiley Infectious Diseases Dermatology http://dx.doi.org/10.1111/jdv.15472 <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Superficial cutaneous infection caused by the zoophilic dermatophyte <jats:italic>Trichophyton benhamiae</jats:italic> is often associated with a highly inflammatory immune response. As non‐professional immune cells, epidermal keratinocytes and dermal fibroblasts contribute to the first line of defence by producing pro‐inflammatory cytokines and antimicrobial peptides (<jats:styled-content style="fixed-case">AMP</jats:styled-content>).</jats:p></jats:sec><jats:sec><jats:title>Objective</jats:title><jats:p>Purpose of this study was to gain a deeper understanding of the pathogenesis and the fungal–host interaction as not much is known about the innate immune response of these cutaneous cells against <jats:italic>T</jats:italic>. <jats:italic>benhamiae</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Using a dermatophytosis model of fibroblasts and keratinocytes incubated with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916, analyses included determination of cell viability and cytotoxicity, effects on the innate immune response including expression and secretion of pro‐inflammatory cytokines/chemokines and expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>, as well as alterations of genes involved in cell adhesion.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>Trichophyton benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection led to severe cell damage and direct induction of a broad spectrum of pro‐inflammatory cytokines and chemokines in both cutaneous cells. Only keratinocytes differentially up‐regulated <jats:styled-content style="fixed-case">AMP</jats:styled-content> genes expression after <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection. Expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>s in fibroblasts was not inducible by fungal infection, whereas their absences potentially contributed to a continuous increase in the fungal biomass on fibroblasts, which in turn was reduced in keratinocytes possibly due to the antimicrobial actions of induced <jats:styled-content style="fixed-case">AMP</jats:styled-content>s. On <jats:styled-content style="fixed-case">mRNA</jats:styled-content> level, <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection altered cell–cell contact proteins in keratinocytes<jats:italic>,</jats:italic> indicating that targeting specific cell–cell adhesion proteins might be part of dermatophytes’ virulence strategy.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>This study showed that in addition to immune cells, keratinocytes and fibroblasts could participate in antimicrobial defence against an exemplary infection with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916.</jats:p></jats:sec> Innate immune response of human epidermal keratinocytes and dermal fibroblasts <i>to in vitro</i> incubation of <i>Trichophyton benhamiae </i><scp>DSM</scp> 6916 Journal of the European Academy of Dermatology and Venereology |
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Wiley, 2019 |
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2019 |
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Journal of the European Academy of Dermatology and Venereology |
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| title |
Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_unstemmed |
Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_full |
Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_fullStr |
Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_full_unstemmed |
Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_short |
Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_sort |
innate immune response of human epidermal keratinocytes and dermal fibroblasts <i>to in vitro</i> incubation of <i>trichophyton benhamiae </i><scp>dsm</scp> 6916 |
| topic |
Infectious Diseases Dermatology |
| url |
http://dx.doi.org/10.1111/jdv.15472 |
| publishDate |
2019 |
| physical |
1177-1188 |
| description |
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Superficial cutaneous infection caused by the zoophilic dermatophyte <jats:italic>Trichophyton benhamiae</jats:italic> is often associated with a highly inflammatory immune response. As non‐professional immune cells, epidermal keratinocytes and dermal fibroblasts contribute to the first line of defence by producing pro‐inflammatory cytokines and antimicrobial peptides (<jats:styled-content style="fixed-case">AMP</jats:styled-content>).</jats:p></jats:sec><jats:sec><jats:title>Objective</jats:title><jats:p>Purpose of this study was to gain a deeper understanding of the pathogenesis and the fungal–host interaction as not much is known about the innate immune response of these cutaneous cells against <jats:italic>T</jats:italic>. <jats:italic>benhamiae</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Using a dermatophytosis model of fibroblasts and keratinocytes incubated with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916, analyses included determination of cell viability and cytotoxicity, effects on the innate immune response including expression and secretion of pro‐inflammatory cytokines/chemokines and expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>, as well as alterations of genes involved in cell adhesion.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>Trichophyton benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection led to severe cell damage and direct induction of a broad spectrum of pro‐inflammatory cytokines and chemokines in both cutaneous cells. Only keratinocytes differentially up‐regulated <jats:styled-content style="fixed-case">AMP</jats:styled-content> genes expression after <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection. Expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>s in fibroblasts was not inducible by fungal infection, whereas their absences potentially contributed to a continuous increase in the fungal biomass on fibroblasts, which in turn was reduced in keratinocytes possibly due to the antimicrobial actions of induced <jats:styled-content style="fixed-case">AMP</jats:styled-content>s. On <jats:styled-content style="fixed-case">mRNA</jats:styled-content> level, <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection altered cell–cell contact proteins in keratinocytes<jats:italic>,</jats:italic> indicating that targeting specific cell–cell adhesion proteins might be part of dermatophytes’ virulence strategy.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>This study showed that in addition to immune cells, keratinocytes and fibroblasts could participate in antimicrobial defence against an exemplary infection with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916.</jats:p></jats:sec> |
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| description | <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Superficial cutaneous infection caused by the zoophilic dermatophyte <jats:italic>Trichophyton benhamiae</jats:italic> is often associated with a highly inflammatory immune response. As non‐professional immune cells, epidermal keratinocytes and dermal fibroblasts contribute to the first line of defence by producing pro‐inflammatory cytokines and antimicrobial peptides (<jats:styled-content style="fixed-case">AMP</jats:styled-content>).</jats:p></jats:sec><jats:sec><jats:title>Objective</jats:title><jats:p>Purpose of this study was to gain a deeper understanding of the pathogenesis and the fungal–host interaction as not much is known about the innate immune response of these cutaneous cells against <jats:italic>T</jats:italic>. <jats:italic>benhamiae</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Using a dermatophytosis model of fibroblasts and keratinocytes incubated with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916, analyses included determination of cell viability and cytotoxicity, effects on the innate immune response including expression and secretion of pro‐inflammatory cytokines/chemokines and expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>, as well as alterations of genes involved in cell adhesion.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>Trichophyton benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection led to severe cell damage and direct induction of a broad spectrum of pro‐inflammatory cytokines and chemokines in both cutaneous cells. Only keratinocytes differentially up‐regulated <jats:styled-content style="fixed-case">AMP</jats:styled-content> genes expression after <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection. Expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>s in fibroblasts was not inducible by fungal infection, whereas their absences potentially contributed to a continuous increase in the fungal biomass on fibroblasts, which in turn was reduced in keratinocytes possibly due to the antimicrobial actions of induced <jats:styled-content style="fixed-case">AMP</jats:styled-content>s. On <jats:styled-content style="fixed-case">mRNA</jats:styled-content> level, <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection altered cell–cell contact proteins in keratinocytes<jats:italic>,</jats:italic> indicating that targeting specific cell–cell adhesion proteins might be part of dermatophytes’ virulence strategy.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>This study showed that in addition to immune cells, keratinocytes and fibroblasts could participate in antimicrobial defence against an exemplary infection with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916.</jats:p></jats:sec> |
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| spelling | Hesse‐Macabata, J. Morgner, B. Morgenstern, S. Grimm, M.O. Elsner, P. Hipler, U.C. Wiegand, C. 0926-9959 1468-3083 Wiley Infectious Diseases Dermatology http://dx.doi.org/10.1111/jdv.15472 <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Superficial cutaneous infection caused by the zoophilic dermatophyte <jats:italic>Trichophyton benhamiae</jats:italic> is often associated with a highly inflammatory immune response. As non‐professional immune cells, epidermal keratinocytes and dermal fibroblasts contribute to the first line of defence by producing pro‐inflammatory cytokines and antimicrobial peptides (<jats:styled-content style="fixed-case">AMP</jats:styled-content>).</jats:p></jats:sec><jats:sec><jats:title>Objective</jats:title><jats:p>Purpose of this study was to gain a deeper understanding of the pathogenesis and the fungal–host interaction as not much is known about the innate immune response of these cutaneous cells against <jats:italic>T</jats:italic>. <jats:italic>benhamiae</jats:italic>.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Using a dermatophytosis model of fibroblasts and keratinocytes incubated with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916, analyses included determination of cell viability and cytotoxicity, effects on the innate immune response including expression and secretion of pro‐inflammatory cytokines/chemokines and expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>, as well as alterations of genes involved in cell adhesion.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>Trichophyton benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection led to severe cell damage and direct induction of a broad spectrum of pro‐inflammatory cytokines and chemokines in both cutaneous cells. Only keratinocytes differentially up‐regulated <jats:styled-content style="fixed-case">AMP</jats:styled-content> genes expression after <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection. Expression of <jats:styled-content style="fixed-case">AMP</jats:styled-content>s in fibroblasts was not inducible by fungal infection, whereas their absences potentially contributed to a continuous increase in the fungal biomass on fibroblasts, which in turn was reduced in keratinocytes possibly due to the antimicrobial actions of induced <jats:styled-content style="fixed-case">AMP</jats:styled-content>s. On <jats:styled-content style="fixed-case">mRNA</jats:styled-content> level, <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916 infection altered cell–cell contact proteins in keratinocytes<jats:italic>,</jats:italic> indicating that targeting specific cell–cell adhesion proteins might be part of dermatophytes’ virulence strategy.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>This study showed that in addition to immune cells, keratinocytes and fibroblasts could participate in antimicrobial defence against an exemplary infection with <jats:italic>T. benhamiae </jats:italic><jats:styled-content style="fixed-case">DSM</jats:styled-content> 6916.</jats:p></jats:sec> Innate immune response of human epidermal keratinocytes and dermal fibroblasts <i>to in vitro</i> incubation of <i>Trichophyton benhamiae </i><scp>DSM</scp> 6916 Journal of the European Academy of Dermatology and Venereology |
| spellingShingle | Hesse‐Macabata, J., Morgner, B., Morgenstern, S., Grimm, M.O., Elsner, P., Hipler, U.C., Wiegand, C., Journal of the European Academy of Dermatology and Venereology, Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916, Infectious Diseases, Dermatology |
| title | Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_full | Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_fullStr | Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_full_unstemmed | Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_short | Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| title_sort | innate immune response of human epidermal keratinocytes and dermal fibroblasts <i>to in vitro</i> incubation of <i>trichophyton benhamiae </i><scp>dsm</scp> 6916 |
| title_unstemmed | Innate immune response of human epidermal keratinocytes and dermal fibroblasts to in vitro incubation of Trichophyton benhamiae DSM 6916 |
| topic | Infectious Diseases, Dermatology |
| url | http://dx.doi.org/10.1111/jdv.15472 |