RapamycinFungusV1, Main, Exploration, bibRecord, 000646

Biguanides enhance antifungal activity against Candida glabrata.

Identifieur interne : 000646 ( Main/Exploration ); précédent : 000645; suivant : 000647

Biguanides enhance antifungal activity against Candida glabrata.

Auteurs : Shuying Xu [États-Unis] ; Marianela Feliu [États-Unis] ; Allison K. Lord [États-Unis] ; Daniel P. Lukason [États-Unis] ; Paige E. Negoro [États-Unis] ; Nida S. Khan [États-Unis] ; Zeina Dagher [États-Unis] ; Michael B. Feldman [États-Unis] ; Jennifer L. Reedy [États-Unis] ; Samantha N. Steiger [États-Unis] ; Jenny M. Tam [États-Unis] ; Alexander A. Soukas [États-Unis] ; David B. Sykes [États-Unis] ; Michael K. Mansour [États-Unis]

Source :

Virulence [ 2150-5608 ] ; 2018.

RBID : pubmed:29962263

Descripteurs français

KwdFr :
- Amphotéricine B (pharmacologie), Antifongiques (pharmacologie), Association médicamenteuse (MeSH), Biguanides (pharmacologie), Candida (effets des médicaments et des substances chimiques), Candida glabrata (croissance et développement), Candida glabrata (effets des médicaments et des substances chimiques), Fluconazole (pharmacologie), Humains (MeSH), Lipopeptides (pharmacologie), Metformine (pharmacologie), Micafungine (MeSH), Mycoses (microbiologie), Mycoses (traitement médicamenteux), Résistance des champignons aux médicaments (MeSH), Sérine-thréonine kinases TOR (effets des médicaments et des substances chimiques), Tests de sensibilité microbienne (MeSH), Voriconazole (pharmacologie), Échinocandines (pharmacologie).
MESH :
- croissance et développement : Candida glabrata.
- effets des médicaments et des substances chimiques : Candida, Candida glabrata, Sérine-thréonine kinases TOR.
- microbiologie : Mycoses.
- pharmacologie : Amphotéricine B, Antifongiques, Biguanides, Fluconazole, Lipopeptides, Metformine, Voriconazole, Échinocandines.
- traitement médicamenteux : Mycoses.
- Association médicamenteuse, Humains, Micafungine, Résistance des champignons aux médicaments, Tests de sensibilité microbienne.

English descriptors

KwdEn :
- Amphotericin B (pharmacology), Antifungal Agents (pharmacology), Biguanides (pharmacology), Candida (drug effects), Candida glabrata (drug effects), Candida glabrata (growth & development), Drug Combinations (MeSH), Drug Resistance, Fungal (MeSH), Echinocandins (pharmacology), Fluconazole (pharmacology), Humans (MeSH), Lipopeptides (pharmacology), Metformin (pharmacology), Micafungin (MeSH), Microbial Sensitivity Tests (MeSH), Mycoses (drug therapy), Mycoses (microbiology), TOR Serine-Threonine Kinases (drug effects), Voriconazole (pharmacology).
MESH :
- chemical , drug effects : TOR Serine-Threonine Kinases.
- chemical , pharmacology : Amphotericin B, Antifungal Agents, Biguanides, Echinocandins, Fluconazole, Lipopeptides, Metformin, Voriconazole.
- drug effects : Candida, Candida glabrata.
- drug therapy : Mycoses.
- growth & development : Candida glabrata.
- microbiology : Mycoses.
- chemical : Drug Combinations, Drug Resistance, Fungal, Humans, Micafungin, Microbial Sensitivity Tests.

Abstract

Candida spp. are the fourth leading cause of nosocomial blood stream infections in North America. Candida glabrata is the second most frequently isolated species, and rapid development of antifungal resistance has made treatment a challenge. In this study, we investigate the therapeutic potential of metformin, a biguanide with well-established action for diabetes, as an antifungal agent against C. glabrata. Both wild type and antifungal-resistant isolates of C. glabrata were subjected to biguanide and biguanide-antifungal combination treatment. Metformin, as well as other members of the biguanide family, were found to have antifungal activity against C. glabrata, with MIC₅₀ of 9.34 ± 0.16 mg/mL, 2.09 ± 0.04 mg/mL and 1.87 ± 0.05 mg/mL for metformin, phenformin and buformin, respectively. We demonstrate that biguanides enhance the activity of several antifungal drugs, including voriconazole, fluconazole, and amphotericin, but not micafungin. The biguanide-antifungal combinations allowed for additional antifungal effects, with fraction inhibition concentration indexes ranging from 0.5 to 1. Furthermore, metformin was able to lower antifungal MIC₅₀ in voriconazole and fluconazole-resistant clinical isolates of C. glabrata. We also observed growth reduction of C. glabrata with rapamycin and an FIC of 0.84 ± 0.09 when combined with metformin, suggesting biguanide action in C. glabrata may be related to inhibition of the mTOR complex. We conclude that the biguanide class has direct antifungal therapeutic potential and enhances the activity of select antifungals in the treatment of resistant C. glabrata isolates. These data support the further investigation of biguanides in the combination treatment of serious fungal infections.

DOI: 10.1080/21505594.2018.1475798
PubMed: 29962263
PubMed Central: PMC6086317

Affiliations:

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

to stream Main, to step Corpus: 000515
to stream Main, to step Curation: 000515

Le document en format XML

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</placeName>
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</placeName>
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</placeName>
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</placeName>
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</placeName>
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<author><name sortKey="Mansour, Michael K" sort="Mansour, Michael K" uniqKey="Mansour M" first="Michael K" last="Mansour">Michael K. Mansour</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Biguanides enhance antifungal activity against Candida glabrata.</title>
<author><name sortKey="Xu, Shuying" sort="Xu, Shuying" uniqKey="Xu S" first="Shuying" last="Xu">Shuying Xu</name>
<affiliation wicri:level="2"><nlm:affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
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<author><name sortKey="Feliu, Marianela" sort="Feliu, Marianela" uniqKey="Feliu M" first="Marianela" last="Feliu">Marianela Feliu</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lord, Allison K" sort="Lord, Allison K" uniqKey="Lord A" first="Allison K" last="Lord">Allison K. Lord</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lukason, Daniel P" sort="Lukason, Daniel P" uniqKey="Lukason D" first="Daniel P" last="Lukason">Daniel P. Lukason</name>
<affiliation wicri:level="2"><nlm:affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Negoro, Paige E" sort="Negoro, Paige E" uniqKey="Negoro P" first="Paige E" last="Negoro">Paige E. Negoro</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
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<author><name sortKey="Khan, Nida S" sort="Khan, Nida S" uniqKey="Khan N" first="Nida S" last="Khan">Nida S. Khan</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>b Biomedical Engineering and Biotechnology , University of Massachusetts Medical School , Worcester , MA , USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>b Biomedical Engineering and Biotechnology , University of Massachusetts Medical School , Worcester , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
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<author><name sortKey="Dagher, Zeina" sort="Dagher, Zeina" uniqKey="Dagher Z" first="Zeina" last="Dagher">Zeina Dagher</name>
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<country xml:lang="fr">États-Unis</country>
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<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Feldman, Michael B" sort="Feldman, Michael B" uniqKey="Feldman M" first="Michael B" last="Feldman">Michael B. Feldman</name>
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<country xml:lang="fr">États-Unis</country>
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<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>d Department of Internal Medicine , Harvard Medical School , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
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<author><name sortKey="Reedy, Jennifer L" sort="Reedy, Jennifer L" uniqKey="Reedy J" first="Jennifer L" last="Reedy">Jennifer L. Reedy</name>
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<country xml:lang="fr">États-Unis</country>
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<placeName><region type="state">Massachusetts</region>
</placeName>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>d Department of Internal Medicine , Harvard Medical School , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Steiger, Samantha N" sort="Steiger, Samantha N" uniqKey="Steiger S" first="Samantha N" last="Steiger">Samantha N. Steiger</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>e Deparment of Pharmacy , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tam, Jenny M" sort="Tam, Jenny M" uniqKey="Tam J" first="Jenny M" last="Tam">Jenny M. Tam</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>d Department of Internal Medicine , Harvard Medical School , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
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<author><name sortKey="Soukas, Alexander A" sort="Soukas, Alexander A" uniqKey="Soukas A" first="Alexander A" last="Soukas">Alexander A. Soukas</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>d Department of Internal Medicine , Harvard Medical School , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>f Diabetes Unit, Department of Endocrinology , Massachusetts General Hospital , Boston , MA , USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>f Diabetes Unit, Department of Endocrinology , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>g Center for Human Genetic Research , Massachusetts General Hospital , Boston , MA , USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>g Center for Human Genetic Research , Massachusetts General Hospital , Boston , MA </wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sykes, David B" sort="Sykes, David B" uniqKey="Sykes D" first="David B" last="Sykes">David B. Sykes</name>
<affiliation wicri:level="2"><nlm:affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>d Department of Internal Medicine , Harvard Medical School , Boston , MA </wicri:regionArea>
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<affiliation wicri:level="2"><nlm:affiliation>h Center for Regenerative Medicine , Massachusetts General Hospital , Boston , MA , USA.</nlm:affiliation>
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<author><name sortKey="Mansour, Michael K" sort="Mansour, Michael K" uniqKey="Mansour M" first="Michael K" last="Mansour">Michael K. Mansour</name>
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<series><title level="j">Virulence</title>
<idno type="eISSN">2150-5608</idno>
<imprint><date when="2018" type="published">2018</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amphotericin B (pharmacology)</term>
<term>Antifungal Agents (pharmacology)</term>
<term>Biguanides (pharmacology)</term>
<term>Candida (drug effects)</term>
<term>Candida glabrata (drug effects)</term>
<term>Candida glabrata (growth & development)</term>
<term>Drug Combinations (MeSH)</term>
<term>Drug Resistance, Fungal (MeSH)</term>
<term>Echinocandins (pharmacology)</term>
<term>Fluconazole (pharmacology)</term>
<term>Humans (MeSH)</term>
<term>Lipopeptides (pharmacology)</term>
<term>Metformin (pharmacology)</term>
<term>Micafungin (MeSH)</term>
<term>Microbial Sensitivity Tests (MeSH)</term>
<term>Mycoses (drug therapy)</term>
<term>Mycoses (microbiology)</term>
<term>TOR Serine-Threonine Kinases (drug effects)</term>
<term>Voriconazole (pharmacology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Amphotéricine B (pharmacologie)</term>
<term>Antifongiques (pharmacologie)</term>
<term>Association médicamenteuse (MeSH)</term>
<term>Biguanides (pharmacologie)</term>
<term>Candida (effets des médicaments et des substances chimiques)</term>
<term>Candida glabrata (croissance et développement)</term>
<term>Candida glabrata (effets des médicaments et des substances chimiques)</term>
<term>Fluconazole (pharmacologie)</term>
<term>Humains (MeSH)</term>
<term>Lipopeptides (pharmacologie)</term>
<term>Metformine (pharmacologie)</term>
<term>Micafungine (MeSH)</term>
<term>Mycoses (microbiologie)</term>
<term>Mycoses (traitement médicamenteux)</term>
<term>Résistance des champignons aux médicaments (MeSH)</term>
<term>Sérine-thréonine kinases TOR (effets des médicaments et des substances chimiques)</term>
<term>Tests de sensibilité microbienne (MeSH)</term>
<term>Voriconazole (pharmacologie)</term>
<term>Échinocandines (pharmacologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Amphotericin B</term>
<term>Antifungal Agents</term>
<term>Biguanides</term>
<term>Echinocandins</term>
<term>Fluconazole</term>
<term>Lipopeptides</term>
<term>Metformin</term>
<term>Voriconazole</term>
</keywords>
<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Candida glabrata</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Candida</term>
<term>Candida glabrata</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Mycoses</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Candida</term>
<term>Candida glabrata</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Candida glabrata</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Mycoses</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Mycoses</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Amphotéricine B</term>
<term>Antifongiques</term>
<term>Biguanides</term>
<term>Fluconazole</term>
<term>Lipopeptides</term>
<term>Metformine</term>
<term>Voriconazole</term>
<term>Échinocandines</term>
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</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Drug Combinations</term>
<term>Drug Resistance, Fungal</term>
<term>Humans</term>
<term>Micafungin</term>
<term>Microbial Sensitivity Tests</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Association médicamenteuse</term>
<term>Humains</term>
<term>Micafungine</term>
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<front><div type="abstract" xml:lang="en">Candida spp. are the fourth leading cause of nosocomial blood stream infections in North America. Candida glabrata is the second most frequently isolated species, and rapid development of antifungal resistance has made treatment a challenge. In this study, we investigate the therapeutic potential of metformin, a biguanide with well-established action for diabetes, as an antifungal agent against C. glabrata. Both wild type and antifungal-resistant isolates of C. glabrata were subjected to biguanide and biguanide-antifungal combination treatment. Metformin, as well as other members of the biguanide family, were found to have antifungal activity against C. glabrata, with MIC<sub>50</sub>
 of 9.34 ± 0.16 mg/mL, 2.09 ± 0.04 mg/mL and 1.87 ± 0.05 mg/mL for metformin, phenformin and buformin, respectively. We demonstrate that biguanides enhance the activity of several antifungal drugs, including voriconazole, fluconazole, and amphotericin, but not micafungin. The biguanide-antifungal combinations allowed for additional antifungal effects, with fraction inhibition concentration indexes ranging from 0.5 to 1. Furthermore, metformin was able to lower antifungal MIC<sub>50</sub>
 in voriconazole and fluconazole-resistant clinical isolates of C. glabrata. We also observed growth reduction of C. glabrata with rapamycin and an FIC of 0.84 ± 0.09 when combined with metformin, suggesting biguanide action in C. glabrata may be related to inhibition of the mTOR complex. We conclude that the biguanide class has direct antifungal therapeutic potential and enhances the activity of select antifungals in the treatment of resistant C. glabrata isolates. These data support the further investigation of biguanides in the combination treatment of serious fungal infections.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>10</Month>
<Day>30</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>10</Month>
<Day>23</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2150-5608</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>9</Volume>
<Issue>1</Issue>
<PubDate><Year>2018</Year>
</PubDate>
</JournalIssue>
<Title>Virulence</Title>
<ISOAbbreviation>Virulence</ISOAbbreviation>
</Journal>
<ArticleTitle>Biguanides enhance antifungal activity against Candida glabrata.</ArticleTitle>
<Pagination><MedlinePgn>1150-1162</MedlinePgn>
</Pagination>
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<Abstract><AbstractText>Candida spp. are the fourth leading cause of nosocomial blood stream infections in North America. Candida glabrata is the second most frequently isolated species, and rapid development of antifungal resistance has made treatment a challenge. In this study, we investigate the therapeutic potential of metformin, a biguanide with well-established action for diabetes, as an antifungal agent against C. glabrata. Both wild type and antifungal-resistant isolates of C. glabrata were subjected to biguanide and biguanide-antifungal combination treatment. Metformin, as well as other members of the biguanide family, were found to have antifungal activity against C. glabrata, with MIC<sub>50</sub>
 of 9.34 ± 0.16 mg/mL, 2.09 ± 0.04 mg/mL and 1.87 ± 0.05 mg/mL for metformin, phenformin and buformin, respectively. We demonstrate that biguanides enhance the activity of several antifungal drugs, including voriconazole, fluconazole, and amphotericin, but not micafungin. The biguanide-antifungal combinations allowed for additional antifungal effects, with fraction inhibition concentration indexes ranging from 0.5 to 1. Furthermore, metformin was able to lower antifungal MIC<sub>50</sub>
 in voriconazole and fluconazole-resistant clinical isolates of C. glabrata. We also observed growth reduction of C. glabrata with rapamycin and an FIC of 0.84 ± 0.09 when combined with metformin, suggesting biguanide action in C. glabrata may be related to inhibition of the mTOR complex. We conclude that the biguanide class has direct antifungal therapeutic potential and enhances the activity of select antifungals in the treatment of resistant C. glabrata isolates. These data support the further investigation of biguanides in the combination treatment of serious fungal infections.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Shuying</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Feliu</LastName>
<ForeName>Marianela</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lord</LastName>
<ForeName>Allison K</ForeName>
<Initials>AK</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lukason</LastName>
<ForeName>Daniel P</ForeName>
<Initials>DP</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Negoro</LastName>
<ForeName>Paige E</ForeName>
<Initials>PE</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Khan</LastName>
<ForeName>Nida S</ForeName>
<Initials>NS</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>b Biomedical Engineering and Biotechnology , University of Massachusetts Medical School , Worcester , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dagher</LastName>
<ForeName>Zeina</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Feldman</LastName>
<ForeName>Michael B</ForeName>
<Initials>MB</Initials>
<AffiliationInfo><Affiliation>c Division of Pulmonary and Critical Care , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Reedy</LastName>
<ForeName>Jennifer L</ForeName>
<Initials>JL</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Steiger</LastName>
<ForeName>Samantha N</ForeName>
<Initials>SN</Initials>
<AffiliationInfo><Affiliation>e Deparment of Pharmacy , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tam</LastName>
<ForeName>Jenny M</ForeName>
<Initials>JM</Initials>
<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</Affiliation>
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<ForeName>Alexander A</ForeName>
<Initials>AA</Initials>
<AffiliationInfo><Affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>f Diabetes Unit, Department of Endocrinology , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>g Center for Human Genetic Research , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>David B</ForeName>
<Initials>DB</Initials>
<Identifier Source="ORCID">0000-0002-9788-0221</Identifier>
<AffiliationInfo><Affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>h Center for Regenerative Medicine , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mansour</LastName>
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<AffiliationInfo><Affiliation>a Division of Infectious Disease , Massachusetts General Hospital , Boston , MA , USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>d Department of Internal Medicine , Harvard Medical School , Boston , MA , USA.</Affiliation>
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<Acronym>CA</Acronym>
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<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
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<Agency>NIA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 HL116275</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AI132638</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
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	Serveur d'exploration sur la rapamycine et les champignons
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Biguanides enhance antifungal activity against Candida glabrata.

Biguanides enhance antifungal activity against Candida glabrata.

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