RapamycinFungusV1, Main, Exploration, bibRecord, 000030

The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection.

Identifieur interne : 000030 ( Main/Exploration ); précédent : 000029; suivant : 000031

The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection.

Auteurs : Chenyu Li [Mexique] ; Cui Li [Mexique] ; Jing Lin [Mexique] ; Guiqiu Zhao [Mexique] ; Qiang Xu [Mexique] ; Nan Jiang [Mexique] ; Qian Wang [Mexique] ; Xudong Peng [Mexique] ; Guoqiang Zhu [Mexique] ; Jiaqian Jiang [Mexique]

Source :

Investigative ophthalmology & visual science [ 1552-5783 ] ; 2020.

RBID : pubmed:32084267

Descripteurs français

KwdFr :
- Animaux (MeSH), Antifongiques (pharmacologie), Aspergillose (anatomopathologie), Aspergillose (immunologie), Aspergillose (métabolisme), Aspergillus fumigatus (immunologie), Autophagie (effets des médicaments et des substances chimiques), Autophagie (immunologie), Cornée (anatomopathologie), Cornée (métabolisme), Immunité innée (immunologie), Kératite (anatomopathologie), Kératite (immunologie), Kératite (métabolisme), Marqueurs biologiques (analyse), Mycoses oculaires (anatomopathologie), Mycoses oculaires (immunologie), Mycoses oculaires (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH).
MESH :
- analyse : Marqueurs biologiques.
- anatomopathologie : Aspergillose, Cornée, Kératite, Mycoses oculaires.
- effets des médicaments et des substances chimiques : Autophagie.
- immunologie : Aspergillose, Aspergillus fumigatus, Autophagie, Immunité innée, Kératite, Mycoses oculaires.
- métabolisme : Aspergillose, Cornée, Kératite, Mycoses oculaires.
- pharmacologie : Antifongiques.
- Animaux, Souris, Souris de lignée C57BL.

English descriptors

KwdEn :
- Animals (MeSH), Antifungal Agents (pharmacology), Aspergillosis (immunology), Aspergillosis (metabolism), Aspergillosis (pathology), Aspergillus fumigatus (immunology), Autophagy (drug effects), Autophagy (immunology), Biomarkers (analysis), Cornea (metabolism), Cornea (pathology), Eye Infections, Fungal (immunology), Eye Infections, Fungal (metabolism), Eye Infections, Fungal (pathology), Immunity, Innate (immunology), Keratitis (immunology), Keratitis (metabolism), Keratitis (pathology), Mice (MeSH), Mice, Inbred C57BL (MeSH).
MESH :
- chemical , analysis : Biomarkers.
- chemical , pharmacology : Antifungal Agents.
- drug effects : Autophagy.
- immunology : Aspergillosis, Aspergillus fumigatus, Autophagy, Eye Infections, Fungal, Immunity, Innate, Keratitis.
- metabolism : Aspergillosis, Cornea, Eye Infections, Fungal, Keratitis.
- pathology : Aspergillosis, Cornea, Eye Infections, Fungal, Keratitis.
- Animals, Mice, Mice, Inbred C57BL.

Abstract

Purpose

To determine the role of autophagy in the innate immune response to fungal keratitis (FK) caused by Aspergillus fumigatus infection.

Methods

Corneal samples obtained from patients and mice with FK were visualized via transmission electron microscopy (TEM). Autophagy-related proteins LC3B-II, Beclin-1, LAMP-1, and p62 in A. fumigatus-infected corneas of C57BL/6 mice were tested by Western blot. After treatment with autophagy inhibitors 3-methyladenine (3-MA), chloroquine (CQ), or inducer rapamycin, autophagy-related proteins were detected by Western blot. Corneas were photographed with slit lamp microscopy and pathological changes were observed by hematoxylin and eosin staining. Polymorphonuclear neutrophilic leukocytes (PMNs) were assessed by immunofluorescent staining and observed under TEM. The levels of CXCL-1, IL-1β, HMGB1, IL-18, TNF-α, and IL-10 were tested by reverse transcription polymerase chain reaction and Western blot. The quantification of fungal loads was detected and photographed.

Results

The accumulation of autophagosomes in corneas of patients and mice with FK was observed with TEM. The expression of LC3B-II, Beclin-1, and LAMP-1 was elevated in corneas after fungal infection, whereas p62 was reduced. Treatment with 3-MA or CQ upregulated clinical scores, pathological changes, and the expression of CXCL-1, IL-1β, HMGB1, IL-18, and TNF-α except IL-10. The morphology of PMNs was changed and PMN recruitment was increased in mice corneas treated with 3-MA or CQ, whereas rapamycin reduced the inflammatory response to keratitis. These results were statistically significant.

Conclusions

A. fumigatus infection increases the expression of autophagy in corneas. Autophagy plays an anti-inflammatory role in the innate immune response to A. fumigatus keratitis.

DOI: 10.1167/iovs.61.2.25
PubMed: 32084267
PubMed Central: PMC7326573

Affiliations:

Mexique

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

to stream Main, to step Corpus: 000112
to stream Main, to step Curation: 000112

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Antifungal Agents (pharmacology)</term>
<term>Aspergillosis (immunology)</term>
<term>Aspergillosis (metabolism)</term>
<term>Aspergillosis (pathology)</term>
<term>Aspergillus fumigatus (immunology)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy (immunology)</term>
<term>Biomarkers (analysis)</term>
<term>Cornea (metabolism)</term>
<term>Cornea (pathology)</term>
<term>Eye Infections, Fungal (immunology)</term>
<term>Eye Infections, Fungal (metabolism)</term>
<term>Eye Infections, Fungal (pathology)</term>
<term>Immunity, Innate (immunology)</term>
<term>Keratitis (immunology)</term>
<term>Keratitis (metabolism)</term>
<term>Keratitis (pathology)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Antifongiques (pharmacologie)</term>
<term>Aspergillose (anatomopathologie)</term>
<term>Aspergillose (immunologie)</term>
<term>Aspergillose (métabolisme)</term>
<term>Aspergillus fumigatus (immunologie)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (immunologie)</term>
<term>Cornée (anatomopathologie)</term>
<term>Cornée (métabolisme)</term>
<term>Immunité innée (immunologie)</term>
<term>Kératite (anatomopathologie)</term>
<term>Kératite (immunologie)</term>
<term>Kératite (métabolisme)</term>
<term>Marqueurs biologiques (analyse)</term>
<term>Mycoses oculaires (anatomopathologie)</term>
<term>Mycoses oculaires (immunologie)</term>
<term>Mycoses oculaires (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Biomarkers</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antifungal Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Marqueurs biologiques</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Aspergillose</term>
<term>Cornée</term>
<term>Kératite</term>
<term>Mycoses oculaires</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Aspergillose</term>
<term>Aspergillus fumigatus</term>
<term>Autophagie</term>
<term>Immunité innée</term>
<term>Kératite</term>
<term>Mycoses oculaires</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aspergillosis</term>
<term>Aspergillus fumigatus</term>
<term>Autophagy</term>
<term>Eye Infections, Fungal</term>
<term>Immunity, Innate</term>
<term>Keratitis</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aspergillosis</term>
<term>Cornea</term>
<term>Eye Infections, Fungal</term>
<term>Keratitis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Aspergillose</term>
<term>Cornée</term>
<term>Kératite</term>
<term>Mycoses oculaires</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aspergillosis</term>
<term>Cornea</term>
<term>Eye Infections, Fungal</term>
<term>Keratitis</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antifongiques</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en"><p><b>Purpose</b>
</p>
<p>To determine the role of autophagy in the innate immune response to fungal keratitis (FK) caused by Aspergillus fumigatus infection.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>Methods</b>
</p>
<p>Corneal samples obtained from patients and mice with FK were visualized via transmission electron microscopy (TEM). Autophagy-related proteins LC3B-II, Beclin-1, LAMP-1, and p62 in A. fumigatus-infected corneas of C57BL/6 mice were tested by Western blot. After treatment with autophagy inhibitors 3-methyladenine (3-MA), chloroquine (CQ), or inducer rapamycin, autophagy-related proteins were detected by Western blot. Corneas were photographed with slit lamp microscopy and pathological changes were observed by hematoxylin and eosin staining. Polymorphonuclear neutrophilic leukocytes (PMNs) were assessed by immunofluorescent staining and observed under TEM. The levels of CXCL-1, IL-1β, HMGB1, IL-18, TNF-α, and IL-10 were tested by reverse transcription polymerase chain reaction and Western blot. The quantification of fungal loads was detected and photographed.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>Results</b>
</p>
<p>The accumulation of autophagosomes in corneas of patients and mice with FK was observed with TEM. The expression of LC3B-II, Beclin-1, and LAMP-1 was elevated in corneas after fungal infection, whereas p62 was reduced. Treatment with 3-MA or CQ upregulated clinical scores, pathological changes, and the expression of CXCL-1, IL-1β, HMGB1, IL-18, and TNF-α except IL-10. The morphology of PMNs was changed and PMN recruitment was increased in mice corneas treated with 3-MA or CQ, whereas rapamycin reduced the inflammatory response to keratitis. These results were statistically significant.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>Conclusions</b>
</p>
<p>A. fumigatus infection increases the expression of autophagy in corneas. Autophagy plays an anti-inflammatory role in the innate immune response to A. fumigatus keratitis.</p>
</div>
</front>
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<DateCompleted><Year>2020</Year>
<Month>04</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>07</Month>
<Day>08</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>61</Volume>
<Issue>2</Issue>
<PubDate><Year>2020</Year>
<Month>02</Month>
<Day>07</Day>
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</JournalIssue>
<Title>Investigative ophthalmology & visual science</Title>
<ISOAbbreviation>Invest Ophthalmol Vis Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection.</ArticleTitle>
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<Abstract><AbstractText Label="Purpose">To determine the role of autophagy in the innate immune response to fungal keratitis (FK) caused by Aspergillus fumigatus infection.</AbstractText>
<AbstractText Label="Methods">Corneal samples obtained from patients and mice with FK were visualized via transmission electron microscopy (TEM). Autophagy-related proteins LC3B-II, Beclin-1, LAMP-1, and p62 in A. fumigatus-infected corneas of C57BL/6 mice were tested by Western blot. After treatment with autophagy inhibitors 3-methyladenine (3-MA), chloroquine (CQ), or inducer rapamycin, autophagy-related proteins were detected by Western blot. Corneas were photographed with slit lamp microscopy and pathological changes were observed by hematoxylin and eosin staining. Polymorphonuclear neutrophilic leukocytes (PMNs) were assessed by immunofluorescent staining and observed under TEM. The levels of CXCL-1, IL-1β, HMGB1, IL-18, TNF-α, and IL-10 were tested by reverse transcription polymerase chain reaction and Western blot. The quantification of fungal loads was detected and photographed.</AbstractText>
<AbstractText Label="Results">The accumulation of autophagosomes in corneas of patients and mice with FK was observed with TEM. The expression of LC3B-II, Beclin-1, and LAMP-1 was elevated in corneas after fungal infection, whereas p62 was reduced. Treatment with 3-MA or CQ upregulated clinical scores, pathological changes, and the expression of CXCL-1, IL-1β, HMGB1, IL-18, and TNF-α except IL-10. The morphology of PMNs was changed and PMN recruitment was increased in mice corneas treated with 3-MA or CQ, whereas rapamycin reduced the inflammatory response to keratitis. These results were statistically significant.</AbstractText>
<AbstractText Label="Conclusions">A. fumigatus infection increases the expression of autophagy in corneas. Autophagy plays an anti-inflammatory role in the innate immune response to A. fumigatus keratitis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Chenyu</ForeName>
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<ForeName>Nan</ForeName>
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	Serveur d'exploration sur la rapamycine et les champignons
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The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection.

The Role of Autophagy in the Innate Immune Response to Fungal Keratitis Caused by Aspergillus fumigatus Infection.

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