PlantImRecepV1, Main, Exploration, bibRecord, 000009

Tryptanthrin promotes keratinocyte and fibroblast responses in vitro after infection with Trichophyton benhamiae DSM6916.

Identifieur interne : 000009 ( Main/Exploration ); précédent : 000008; suivant : 000010

Tryptanthrin promotes keratinocyte and fibroblast responses in vitro after infection with Trichophyton benhamiae DSM6916.

Auteurs : Jana Hesse-Macabata [Allemagne] ; Bianka Morgner [Allemagne] ; Peter Elsner [Allemagne] ; Uta-Christina Hipler [Allemagne] ; Cornelia Wiegand [Allemagne]

Source :

Scientific reports [ 2045-2322 ] ; 2020.

RBID : pubmed:32024909

Descripteurs français

KwdFr :
- Antigène KI-67 (métabolisme), Cytokines (métabolisme), Fibroblastes (effets des médicaments et des substances chimiques), Fibroblastes (microbiologie), Fibroblastes (métabolisme), Humains (MeSH), Immunité innée (effets des médicaments et des substances chimiques), Inflammation (microbiologie), Inflammation (métabolisme), Inflammation (traitement médicamenteux), Kératinocytes (effets des médicaments et des substances chimiques), Kératinocytes (microbiologie), Kératinocytes (métabolisme), Lignée cellulaire (MeSH), Peau (effets des médicaments et des substances chimiques), Peau (microbiologie), Peau (métabolisme), Peptides antimicrobiens cationiques (métabolisme), Quinazolines (pharmacologie), Récepteur de type Toll-2 (métabolisme), Teigne (microbiologie), Teigne (métabolisme), Teigne (traitement médicamenteux), Trichophyton (effets des médicaments et des substances chimiques), Épiderme (effets des médicaments et des substances chimiques), Épiderme (microbiologie), Épiderme (métabolisme).
MESH :
- effets des médicaments et des substances chimiques : Fibroblastes, Immunité innée, Kératinocytes, Peau, Trichophyton, Épiderme.
- microbiologie : Fibroblastes, Inflammation, Kératinocytes, Peau, Teigne, Épiderme.
- métabolisme : Antigène KI-67, Cytokines, Fibroblastes, Inflammation, Kératinocytes, Peau, Peptides antimicrobiens cationiques, Récepteur de type Toll-2, Teigne, Épiderme.
- pharmacologie : Quinazolines.
- traitement médicamenteux : Inflammation, Teigne.
- Humains, Lignée cellulaire.

English descriptors

KwdEn :
- Antimicrobial Cationic Peptides (metabolism), Cell Line (MeSH), Cytokines (metabolism), Epidermis (drug effects), Epidermis (metabolism), Epidermis (microbiology), Fibroblasts (drug effects), Fibroblasts (metabolism), Fibroblasts (microbiology), Humans (MeSH), Immunity, Innate (drug effects), Inflammation (drug therapy), Inflammation (metabolism), Inflammation (microbiology), Keratinocytes (drug effects), Keratinocytes (metabolism), Keratinocytes (microbiology), Ki-67 Antigen (metabolism), Quinazolines (pharmacology), Skin (drug effects), Skin (metabolism), Skin (microbiology), Tinea (drug therapy), Tinea (metabolism), Tinea (microbiology), Toll-Like Receptor 2 (metabolism), Trichophyton (drug effects).
MESH :
- chemical , metabolism : Antimicrobial Cationic Peptides, Cytokines, Ki-67 Antigen, Toll-Like Receptor 2.
- drug effects : Epidermis, Fibroblasts, Immunity, Innate, Keratinocytes, Skin, Trichophyton.
- drug therapy : Inflammation, Tinea.
- metabolism : Epidermis, Fibroblasts, Inflammation, Keratinocytes, Skin, Tinea.
- microbiology : Epidermis, Fibroblasts, Inflammation, Keratinocytes, Skin, Tinea.
- chemical , pharmacology : Quinazolines.
- Cell Line, Humans.

Abstract

Exceedingly virulent pathogens and growing antimicrobial resistances require new therapeutic approaches. The zoophilic dermatophyte Trichophyton benhamiae causes highly inflammatory, cutaneous fungal infections. Recently, it could be shown that the plant-derived alkaloid tryptanthrin (TRP) exhibits strong anti-microbial activities against yeasts and dermatophytes. The aim of this study was to analyse the bioactivity of TRP under infectious conditions using an in-vitro dermatophytosis model employing fibroblasts and keratinocytes infected with T. benhamiae DSM6916. Analyses comprised determination of cell viability, effects on the innate immune response including expression and secretion of pro-inflammatory cytokines/chemokines as well as expression of various antimicrobial peptides (AMP), toll-like receptor (TLR) 2 and proliferation marker MKI67. T. benhamiae caused severe inflammation in the cutaneous cell models. TRP almost fully prevented T. benhamiae-derived damage of dermal fibroblasts and substantially reduced it in epidermal keratinocytes. A distinct down-regulation of the expression and secretion of pro-inflammatory cytokines was observed. Further, TRP promoted AMP expression, especially of HBD2 and HBD3, in keratinocytes even without fungal presence. This study provides crucial evidence that TRP is not only a strong antifungal agent but also potentially modulates the innate immune response. This makes it interesting as a natural antimycotic drug for adjuvant treatment and prevention of fungal re-infection.

DOI: 10.1038/s41598-020-58773-2
PubMed: 32024909
PubMed Central: PMC7002663

Affiliations:

Allemagne

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000223
to stream Main, to step Curation: 000223

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antimicrobial Cationic Peptides (metabolism)</term>
<term>Cell Line (MeSH)</term>
<term>Cytokines (metabolism)</term>
<term>Epidermis (drug effects)</term>
<term>Epidermis (metabolism)</term>
<term>Epidermis (microbiology)</term>
<term>Fibroblasts (drug effects)</term>
<term>Fibroblasts (metabolism)</term>
<term>Fibroblasts (microbiology)</term>
<term>Humans (MeSH)</term>
<term>Immunity, Innate (drug effects)</term>
<term>Inflammation (drug therapy)</term>
<term>Inflammation (metabolism)</term>
<term>Inflammation (microbiology)</term>
<term>Keratinocytes (drug effects)</term>
<term>Keratinocytes (metabolism)</term>
<term>Keratinocytes (microbiology)</term>
<term>Ki-67 Antigen (metabolism)</term>
<term>Quinazolines (pharmacology)</term>
<term>Skin (drug effects)</term>
<term>Skin (metabolism)</term>
<term>Skin (microbiology)</term>
<term>Tinea (drug therapy)</term>
<term>Tinea (metabolism)</term>
<term>Tinea (microbiology)</term>
<term>Toll-Like Receptor 2 (metabolism)</term>
<term>Trichophyton (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Antigène KI-67 (métabolisme)</term>
<term>Cytokines (métabolisme)</term>
<term>Fibroblastes (effets des médicaments et des substances chimiques)</term>
<term>Fibroblastes (microbiologie)</term>
<term>Fibroblastes (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Immunité innée (effets des médicaments et des substances chimiques)</term>
<term>Inflammation (microbiologie)</term>
<term>Inflammation (métabolisme)</term>
<term>Inflammation (traitement médicamenteux)</term>
<term>Kératinocytes (effets des médicaments et des substances chimiques)</term>
<term>Kératinocytes (microbiologie)</term>
<term>Kératinocytes (métabolisme)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Peau (effets des médicaments et des substances chimiques)</term>
<term>Peau (microbiologie)</term>
<term>Peau (métabolisme)</term>
<term>Peptides antimicrobiens cationiques (métabolisme)</term>
<term>Quinazolines (pharmacologie)</term>
<term>Récepteur de type Toll-2 (métabolisme)</term>
<term>Teigne (microbiologie)</term>
<term>Teigne (métabolisme)</term>
<term>Teigne (traitement médicamenteux)</term>
<term>Trichophyton (effets des médicaments et des substances chimiques)</term>
<term>Épiderme (effets des médicaments et des substances chimiques)</term>
<term>Épiderme (microbiologie)</term>
<term>Épiderme (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antimicrobial Cationic Peptides</term>
<term>Cytokines</term>
<term>Ki-67 Antigen</term>
<term>Toll-Like Receptor 2</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Epidermis</term>
<term>Fibroblasts</term>
<term>Immunity, Innate</term>
<term>Keratinocytes</term>
<term>Skin</term>
<term>Trichophyton</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Inflammation</term>
<term>Tinea</term>
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<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Fibroblastes</term>
<term>Immunité innée</term>
<term>Kératinocytes</term>
<term>Peau</term>
<term>Trichophyton</term>
<term>Épiderme</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epidermis</term>
<term>Fibroblasts</term>
<term>Inflammation</term>
<term>Keratinocytes</term>
<term>Skin</term>
<term>Tinea</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Fibroblastes</term>
<term>Inflammation</term>
<term>Kératinocytes</term>
<term>Peau</term>
<term>Teigne</term>
<term>Épiderme</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Epidermis</term>
<term>Fibroblasts</term>
<term>Inflammation</term>
<term>Keratinocytes</term>
<term>Skin</term>
<term>Tinea</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigène KI-67</term>
<term>Cytokines</term>
<term>Fibroblastes</term>
<term>Inflammation</term>
<term>Kératinocytes</term>
<term>Peau</term>
<term>Peptides antimicrobiens cationiques</term>
<term>Récepteur de type Toll-2</term>
<term>Teigne</term>
<term>Épiderme</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Quinazolines</term>
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<term>Humans</term>
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<front><div type="abstract" xml:lang="en">Exceedingly virulent pathogens and growing antimicrobial resistances require new therapeutic approaches. The zoophilic dermatophyte Trichophyton benhamiae causes highly inflammatory, cutaneous fungal infections. Recently, it could be shown that the plant-derived alkaloid tryptanthrin (TRP) exhibits strong anti-microbial activities against yeasts and dermatophytes. The aim of this study was to analyse the bioactivity of TRP under infectious conditions using an in-vitro dermatophytosis model employing fibroblasts and keratinocytes infected with T. benhamiae DSM6916. Analyses comprised determination of cell viability, effects on the innate immune response including expression and secretion of pro-inflammatory cytokines/chemokines as well as expression of various antimicrobial peptides (AMP), toll-like receptor (TLR) 2 and proliferation marker MKI67. T. benhamiae caused severe inflammation in the cutaneous cell models. TRP almost fully prevented T. benhamiae-derived damage of dermal fibroblasts and substantially reduced it in epidermal keratinocytes. A distinct down-regulation of the expression and secretion of pro-inflammatory cytokines was observed. Further, TRP promoted AMP expression, especially of HBD2 and HBD3, in keratinocytes even without fungal presence. This study provides crucial evidence that TRP is not only a strong antifungal agent but also potentially modulates the innate immune response. This makes it interesting as a natural antimycotic drug for adjuvant treatment and prevention of fungal re-infection.</div>
</front>
</TEI>
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<Abstract><AbstractText>Exceedingly virulent pathogens and growing antimicrobial resistances require new therapeutic approaches. The zoophilic dermatophyte Trichophyton benhamiae causes highly inflammatory, cutaneous fungal infections. Recently, it could be shown that the plant-derived alkaloid tryptanthrin (TRP) exhibits strong anti-microbial activities against yeasts and dermatophytes. The aim of this study was to analyse the bioactivity of TRP under infectious conditions using an in-vitro dermatophytosis model employing fibroblasts and keratinocytes infected with T. benhamiae DSM6916. Analyses comprised determination of cell viability, effects on the innate immune response including expression and secretion of pro-inflammatory cytokines/chemokines as well as expression of various antimicrobial peptides (AMP), toll-like receptor (TLR) 2 and proliferation marker MKI67. T. benhamiae caused severe inflammation in the cutaneous cell models. TRP almost fully prevented T. benhamiae-derived damage of dermal fibroblasts and substantially reduced it in epidermal keratinocytes. A distinct down-regulation of the expression and secretion of pro-inflammatory cytokines was observed. Further, TRP promoted AMP expression, especially of HBD2 and HBD3, in keratinocytes even without fungal presence. This study provides crucial evidence that TRP is not only a strong antifungal agent but also potentially modulates the innate immune response. This makes it interesting as a natural antimycotic drug for adjuvant treatment and prevention of fungal re-infection.</AbstractText>
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<ForeName>Jana</ForeName>
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<AffiliationInfo><Affiliation>Department of Dermatology, Jena University Hospital, Jena, Germany.</Affiliation>
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<ForeName>Bianka</ForeName>
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<ForeName>Peter</ForeName>
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<AffiliationInfo><Affiliation>Department of Dermatology, Jena University Hospital, Jena, Germany.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wiegand</LastName>
<ForeName>Cornelia</ForeName>
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<Identifier Source="ORCID">0000-0001-7802-2785</Identifier>
<AffiliationInfo><Affiliation>Department of Dermatology, Jena University Hospital, Jena, Germany. c.wiegand@med.uni-jena.de.</Affiliation>
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	Serveur d'exploration sur les récepteurs immunitaires végétaux
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Tryptanthrin promotes keratinocyte and fibroblast responses in vitro after infection with Trichophyton benhamiae DSM6916.

Tryptanthrin promotes keratinocyte and fibroblast responses in vitro after infection with Trichophyton benhamiae DSM6916.

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