Inhibition of Respiration of Candida albicans by Small Molecules Increases Phagocytosis Efficacy by Macrophages
The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans , as the coverage of the β-glucan layer by mannans is one...
Uloženo v:
| Vydáno v: | mSphere Ročník 5; číslo 2 |
|---|---|
| Hlavní autoři: | , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
American Society for Microbiology
15.04.2020
|
| Témata: | |
| ISSN: | 2379-5042, 2379-5042 |
| On-line přístup: | Získat plný text |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | The yeast
Candida albicans
is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of
C. albicans
, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc
1
complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability.
Candida albicans
adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of
C. albicans
and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc
1
complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions.
IMPORTANCE
The yeast
Candida albicans
is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of
C. albicans
, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc
1
complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. |
|---|---|
| AbstractList | Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc1 complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions.IMPORTANCE The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability.Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc1 complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions.IMPORTANCE The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. ABSTRACT Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc1 complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions. IMPORTANCE The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. ABSTRACTCandida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc1 complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions.IMPORTANCE The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc1 complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions. IMPORTANCE The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans, as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions. The yeast is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of , as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans , as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc 1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not only allow survival but also influence the interaction with host cells, which is governed by the composition and structure of the fungal cell wall. Numerous studies had shown linkages between mitochondrial functionality, cell wall integrity and structure, and pathogenicity. Thus, we decided to inhibit single complexes of the respiratory chain of C. albicans and to analyze the resultant interaction with macrophages via their phagocytic activity. Remarkably, inhibition of the fungal bc 1 complex by antimycin A increased phagocytosis, which correlated with an increased accessibility of β-glucans. To contribute to mechanistic insights, we performed metabolic studies, which highlighted significant changes in the abundance of constituents of the plasma membrane. Collectively, our results reinforce the strong linkage between fungal energy metabolism and other components of fungal physiology, which also determine the vulnerability to immune defense reactions. IMPORTANCE The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the phagocytosis efficacy of macrophages by targeting the cell wall structure of C. albicans , as the coverage of the β-glucan layer by mannans is one of the immune escape mechanisms of the fungus. We unambiguously show that inhibition of the fungal bc 1 complex correlates with increased accessibilities of β-glucans and improved phagocytosis efficiency. Metabolic studies proved not only the known direct effects on reactive oxygen species (ROS) production and fermentative pathways but also the clear downregulation of the ergosterol pathway and upregulation of unsaturated fatty acids. The changed composition of the plasma membrane could also influence the interaction with the overlying cell wall. Thus, our work highlights the far-reaching relevance of energy metabolism, indirectly also for host-pathogen interactions, without affecting viability. |
| Author | Wang, Junsong Hassan, Rabeay Y. A. Cui, Shuna Li, Minghui Heintz-Buschart, Anna Bilitewski, Ursula |
| Author_xml | – sequence: 1 givenname: Shuna orcidid: 0000-0003-2011-0314 surname: Cui fullname: Cui, Shuna organization: Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Medical College of Yangzhou University, Yangzhou, China, Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany, Department of Obstetrics and Gynecology, Affiliated Hospital of Yangzhou University, Yangzhou, China, Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou, China – sequence: 2 givenname: Minghui surname: Li fullname: Li, Minghui organization: School of Environmental and Biological Engineering, Nanjing University of Science and Technology, Nanjing, China – sequence: 3 givenname: Rabeay Y. A. surname: Hassan fullname: Hassan, Rabeay Y. A. organization: Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany, Center for Materials Sciences, Zewail City of Science and Technology, Giza, Egypt, Applied Organic Chemistry Department, National Research Centre (NRC), Giza, Egypt – sequence: 4 givenname: Anna surname: Heintz-Buschart fullname: Heintz-Buschart, Anna organization: Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany, Department of Soil Ecology, Helmholtz-Centre for Environmental Research GmbH—UFZ, Halle/Saale, Germany, German Centre for Integrative Biodiversity Research (iDiv) Halle-Jena-Leipzig, Leipzig, Germany – sequence: 5 givenname: Junsong surname: Wang fullname: Wang, Junsong organization: School of Environmental and Biological Engineering, Nanjing University of Science and Technology, Nanjing, China – sequence: 6 givenname: Ursula surname: Bilitewski fullname: Bilitewski, Ursula organization: Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32295866$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1kt9rFDEQxxep2Fr77pMs-OLL1iS7SW5fBDmqHrQoVp_DJJm9y5FLzmSvcP-9uV_SFnwImWS-3w_DzLyuzkIMWFVvKbmmlE0-ru7XC0x4TQihomHkRXXBWtk3nHTs7FF8Xl3lvNyrmBBSvKrOW8Z6PhHiooqzsHDajS6GOg71T8xrl-D0nEKwzkINXjsDIdd6W9-vwPv6Lno0G4-5ngWTEHKJfixgHs12jNnl-mYYisVsd5Y7MCmuSxbzm-rlAD7j1fG-rH5_ufk1_dbcfv86m36-bUzXk7GxXAorhgkI1Eh73QqtDaVcd0CxxZaCJHwgHLklUlJtbG-4ZkAsIwiWtpfV7MC1EZZqndwK0lZFcGr_EdNcQRqd8ah6zjopGW0p0R3HXpczkZwwa4yhUhfWpwNrvdErtAbDmMA_gT7NBLdQ8_igJBVESFkAH46AFP9sMI9q5bJB7yFg3GTF2p4ITiXjRfr-mXQZNymUVu1Uou_6TpKieve4on-lnOZaBOIgKI3POeGgjBv3Yy0FOq8oUbsdUscdUvvtUGxHJs-MJ_Z_LX8B2H3MRA |
| CitedBy_id | crossref_primary_10_3390_biom14060670 crossref_primary_10_3390_s21041279 crossref_primary_10_1016_j_fbr_2025_100448 crossref_primary_10_3390_jof11040271 crossref_primary_10_1016_j_micpath_2023_106507 crossref_primary_10_3390_molecules26092549 |
| Cites_doi | 10.1038/nri1745 10.1128/JB.105.1.1-5.1971 10.1186/s12951-015-0147-8 10.1128/AAC.01520-12 10.1111/cmi.12135 10.1016/j.ab.2011.07.025 10.1007/s10863-006-9012-7 10.1371/journal.ppat.1005133 10.1371/journal.ppat.1006403 10.1111/j.1365-2958.2010.07503.x 10.1128/EC.00105-08 10.1021/pr4002178 10.1007/s11306-014-0715-1 10.1128/IAI.00989-09 10.1093/nar/gkp836 10.1111/mmi.13020 10.1128/AEM.02765-05 10.1084/jem.20021890 10.1111/cmi.12438 10.1615/CritRevImmunol.v24.i3.30 10.1093/femsyr/fov027 10.1007/s00294-019-01001-w 10.1093/genetics/134.3.717 10.1371/journal.ppat.0020035 10.1128/mBio.02535-18 10.1080/00032710701327047 10.1128/mBio.01318-18 10.14336/AD.2018.1027 10.1038/nrmicro1815 10.1099/mic.0.040006-0 10.1128/IAI.01612-14 10.4049/jimmunol.177.7.4679 10.1016/j.mito.2017.08.003 10.1080/21505594.2016.1188235 10.1021/acs.jproteome.6b00800 10.1371/journal.pgen.1007892 10.1111/j.1365-2672.2009.04443.x |
| ContentType | Journal Article |
| Copyright | Copyright © 2020 Cui et al. Copyright © 2020 Cui et al. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2020 Cui et al. 2020 Cui et al. |
| Copyright_xml | – notice: Copyright © 2020 Cui et al. – notice: Copyright © 2020 Cui et al. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Copyright © 2020 Cui et al. 2020 Cui et al. |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7X7 7XB 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M7P PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS 7X8 5PM DOA |
| DOI | 10.1128/mSphere.00016-20 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) ProQuest - Health & Medical Complete保健、医学与药学数据库 ProQuest Central (purchase pre-March 2016) ProQuest SciTech Collection ProQuest Natural Science Collection ProQuest Hospital Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central ProQuest Central Essentials - QC Biological Science Collection Proquest Central Natural Science Collection ProQuest One ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Biological Science Database ProQuest Central Premium ProQuest One Academic ProQuest - Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Biological Science Collection ProQuest Central (New) ProQuest Biological Science Collection ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic Publicly Available Content Database MEDLINE CrossRef |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: PIMPY name: Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| DocumentTitleAlternate | Responses to Mitochondrial bc1 Complex Inhibition |
| EISSN | 2379-5042 |
| ExternalDocumentID | oai_doaj_org_article_95247721310b45e9b5e987502dccc17b PMC7160677 32295866 10_1128_mSphere_00016_20 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: ; grantid: 81703969 |
| GroupedDBID | 0R~ 53G 5VS 7X7 8FE 8FH 8FI 8FJ AAFWJ AAGFI AAUOK AAYXX ABUWG ADBBV AFFHD AFKRA AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BBNVY BCNDV BENPR BHPHI BPHCQ BVXVI CCPQU CITATION DIK EBS FRP FYUFA GROUPED_DOAJ H13 HCIFZ HMCUK HYE KQ8 LK8 M48 M7P M~E O9- OK1 PGMZT PHGZM PHGZT PIMPY PQGLB PQQKQ PROAC R9- RHI RPM RSF UKHRP ALIPV CGR CUY CVF ECM EIF NPM 3V. 7XB 8FK AZQEC DWQXO GNUQQ K9. PJZUB PKEHL PPXIY PQEST PQUKI PRINS 7X8 5PM |
| ID | FETCH-LOGICAL-c490t-d576d6f8a6ebe19b36bbc115b4a1e3e31a705f05e5d0771bcd9c5b2a0d20ead13 |
| IEDL.DBID | DOA |
| ISICitedReferencesCount | 10 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000551068100013&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 2379-5042 |
| IngestDate | Mon Nov 10 04:35:53 EST 2025 Tue Nov 04 02:04:45 EST 2025 Sun Nov 09 09:24:54 EST 2025 Sat Nov 01 15:07:46 EDT 2025 Mon Jul 21 06:05:31 EDT 2025 Tue Nov 18 20:53:24 EST 2025 Sat Nov 29 03:33:44 EST 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Keywords | antimycin A phagocytosis metabolism complex III respiratory chain |
| Language | English |
| License | Copyright © 2020 Cui et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c490t-d576d6f8a6ebe19b36bbc115b4a1e3e31a705f05e5d0771bcd9c5b2a0d20ead13 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Citation Cui S, Li M, Hassan RYA, Heintz-Buschart A, Wang J, Bilitewski U. 2020. Inhibition of respiration of Candida albicans by small molecules increases phagocytosis efficacy by macrophages. mSphere 5:e00016-20. https://doi.org/10.1128/mSphere.00016-20. |
| ORCID | 0000-0003-2011-0314 |
| OpenAccessLink | https://doaj.org/article/95247721310b45e9b5e987502dccc17b |
| PMID | 32295866 |
| PQID | 2396949470 |
| PQPubID | 2045592 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_95247721310b45e9b5e987502dccc17b pubmedcentral_primary_oai_pubmedcentral_nih_gov_7160677 proquest_miscellaneous_2390651725 proquest_journals_2396949470 pubmed_primary_32295866 crossref_citationtrail_10_1128_mSphere_00016_20 crossref_primary_10_1128_mSphere_00016_20 |
| PublicationCentury | 2000 |
| PublicationDate | 20200415 |
| PublicationDateYYYYMMDD | 2020-04-15 |
| PublicationDate_xml | – month: 4 year: 2020 text: 20200415 day: 15 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: Washington – name: 1752 N St., N.W., Washington, DC |
| PublicationTitle | mSphere |
| PublicationTitleAlternate | mSphere |
| PublicationYear | 2020 |
| Publisher | American Society for Microbiology |
| Publisher_xml | – name: American Society for Microbiology |
| References | e_1_3_2_26_2 e_1_3_2_27_2 e_1_3_2_28_2 e_1_3_2_29_2 e_1_3_2_20_2 e_1_3_2_21_2 e_1_3_2_22_2 e_1_3_2_23_2 e_1_3_2_24_2 e_1_3_2_25_2 e_1_3_2_9_2 e_1_3_2_15_2 e_1_3_2_38_2 e_1_3_2_8_2 e_1_3_2_16_2 e_1_3_2_37_2 e_1_3_2_7_2 e_1_3_2_17_2 e_1_3_2_6_2 e_1_3_2_18_2 e_1_3_2_19_2 e_1_3_2_30_2 e_1_3_2_32_2 e_1_3_2_10_2 e_1_3_2_31_2 e_1_3_2_5_2 e_1_3_2_11_2 e_1_3_2_34_2 e_1_3_2_4_2 e_1_3_2_12_2 e_1_3_2_33_2 e_1_3_2_3_2 e_1_3_2_13_2 e_1_3_2_36_2 e_1_3_2_2_2 e_1_3_2_14_2 e_1_3_2_35_2 |
| References_xml | – ident: e_1_3_2_18_2 doi: 10.1038/nri1745 – ident: e_1_3_2_32_2 doi: 10.1128/JB.105.1.1-5.1971 – ident: e_1_3_2_34_2 doi: 10.1186/s12951-015-0147-8 – ident: e_1_3_2_27_2 doi: 10.1128/AAC.01520-12 – ident: e_1_3_2_13_2 doi: 10.1111/cmi.12135 – ident: e_1_3_2_16_2 doi: 10.1016/j.ab.2011.07.025 – ident: e_1_3_2_20_2 doi: 10.1007/s10863-006-9012-7 – ident: e_1_3_2_24_2 doi: 10.1371/journal.ppat.1005133 – ident: e_1_3_2_4_2 doi: 10.1371/journal.ppat.1006403 – ident: e_1_3_2_28_2 doi: 10.1111/j.1365-2958.2010.07503.x – ident: e_1_3_2_21_2 doi: 10.1128/EC.00105-08 – ident: e_1_3_2_35_2 doi: 10.1021/pr4002178 – ident: e_1_3_2_38_2 doi: 10.1007/s11306-014-0715-1 – ident: e_1_3_2_6_2 doi: 10.1128/IAI.00989-09 – ident: e_1_3_2_33_2 doi: 10.1093/nar/gkp836 – ident: e_1_3_2_3_2 doi: 10.1111/mmi.13020 – ident: e_1_3_2_29_2 doi: 10.1128/AEM.02765-05 – ident: e_1_3_2_17_2 doi: 10.1084/jem.20021890 – ident: e_1_3_2_14_2 doi: 10.1111/cmi.12438 – ident: e_1_3_2_19_2 doi: 10.1615/CritRevImmunol.v24.i3.30 – ident: e_1_3_2_26_2 doi: 10.1093/femsyr/fov027 – ident: e_1_3_2_15_2 doi: 10.1007/s00294-019-01001-w – ident: e_1_3_2_30_2 doi: 10.1093/genetics/134.3.717 – ident: e_1_3_2_9_2 doi: 10.1371/journal.ppat.0020035 – ident: e_1_3_2_11_2 doi: 10.1128/mBio.02535-18 – ident: e_1_3_2_5_2 doi: 10.1080/00032710701327047 – ident: e_1_3_2_12_2 doi: 10.1128/mBio.01318-18 – ident: e_1_3_2_37_2 doi: 10.14336/AD.2018.1027 – ident: e_1_3_2_2_2 doi: 10.1038/nrmicro1815 – ident: e_1_3_2_8_2 doi: 10.1099/mic.0.040006-0 – ident: e_1_3_2_10_2 doi: 10.1128/IAI.01612-14 – ident: e_1_3_2_31_2 doi: 10.4049/jimmunol.177.7.4679 – ident: e_1_3_2_23_2 doi: 10.1016/j.mito.2017.08.003 – ident: e_1_3_2_25_2 doi: 10.1080/21505594.2016.1188235 – ident: e_1_3_2_36_2 doi: 10.1021/acs.jproteome.6b00800 – ident: e_1_3_2_7_2 doi: 10.1371/journal.pgen.1007892 – ident: e_1_3_2_22_2 doi: 10.1111/j.1365-2672.2009.04443.x |
| SSID | ssj0001626676 |
| Score | 2.1839893 |
| Snippet | The yeast
Candida albicans
is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the... adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive reactions not... ABSTRACTCandida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These... Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These adaptive... The yeast Candida albicans is one of the major fungal human pathogens, for which new therapeutic approaches are required. We aimed at enhancements of the... ABSTRACT Candida albicans adapts to various conditions in different body niches by regulating gene expression, protein synthesis, and metabolic pathways. These... |
| SourceID | doaj pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| SubjectTerms | Animals Antifungal Agents - pharmacology Antimycin A Antimycin A - pharmacology Candida albicans Candida albicans - drug effects Candida albicans - metabolism Cell walls Cells, Cultured complex III Efficiency Electron Transport Energy Metabolism Ergosterol Experiments Fatty acids Fungi Gene expression Glucans Host-pathogen interactions Immune system Influence Kinases Macrophages Macrophages - microbiology Metabolic pathways metabolism Mice Mitochondria Pathogenicity Pathogens Phagocytes Phagocytosis Protein biosynthesis Proteins RAW 264.7 Cells Reactive oxygen species Respiration respiratory chain Signal transduction Standard deviation Therapeutics and Prevention β-Glucan |
| SummonAdditionalLinks | – databaseName: Biological Science Database dbid: M7P link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Jb9QwFLaggMSFHRooyEhcOIRx7NiOTwiqVnBoNaIg9RZ5S2ekaVIm00rz7_FzPGkHoV44REpiW3rS8_I2fx9CH8KpXlWe6twVVZOXgPcZ_BCWc2VEwyRvpG4i2YQ8Pq5OT9U0Bdz6VFa52RPjRu06CzHyCWVKqFKVkny--J0DaxRkVxOFxl10D1ASaCzdm17HWIK1LuSYnaTV5PwELuv7T7ExB5LvG6dRBO3_l6X5d8HkjRPo8PH_yv4EPUq2J_4yTJan6I5vn6EHAxvl-jnqvrezuYklXLhr8I-UhE-f-3D_xWmsFwZ2zh6bNT4514sFPhoYdn2Pw2YDNe7hbTrTZ51dr7p-3uMDgKnQdg1DjjRwhoVW379Avw4Pfu5_yxMfQ25LRVa5C76JE02lRdB8oQwTxthgUZpSFx6CqVoS3hDuuSNSFsY6ZbmhmjhKwoQt2Eu003at30WYE6eDbaR5A2lQwbSTlWGslI0u4bZshiYbvdQ2gZUDZ8aijk4LreqkyZg8FzUlGfo4jrgYgDpu6fsVVD32A4jt-KNbntVpxdaK0zK4HkWwf03JvTLhCc4doc5aW0iTob2Nsuu07vv6WtMZej82hxULaRjd-u4y9gl2XzAceYZeDfNqlIQBu3olRIbk1ozbEnW7pZ3PIip4cHwBDfD17WK9QQ8pRAwArZLvoZ3V8tK_Rfft1WreL9_F5fMHLVsm6A priority: 102 providerName: ProQuest |
| Title | Inhibition of Respiration of Candida albicans by Small Molecules Increases Phagocytosis Efficacy by Macrophages |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/32295866 https://www.proquest.com/docview/2396949470 https://www.proquest.com/docview/2390651725 https://pubmed.ncbi.nlm.nih.gov/PMC7160677 https://doaj.org/article/95247721310b45e9b5e987502dccc17b |
| Volume | 5 |
| WOSCitedRecordID | wos000551068100013&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 2379-5042 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0001626676 issn: 2379-5042 databaseCode: DOA dateStart: 20160101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 2379-5042 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0001626676 issn: 2379-5042 databaseCode: M~E dateStart: 20160101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre – providerCode: PRVPQU databaseName: Biological Science Database customDbUrl: eissn: 2379-5042 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0001626676 issn: 2379-5042 databaseCode: M7P dateStart: 20150101 isFulltext: true titleUrlDefault: http://search.proquest.com/biologicalscijournals providerName: ProQuest – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 2379-5042 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0001626676 issn: 2379-5042 databaseCode: 7X7 dateStart: 20150101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 2379-5042 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0001626676 issn: 2379-5042 databaseCode: BENPR dateStart: 20150101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 2379-5042 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0001626676 issn: 2379-5042 databaseCode: PIMPY dateStart: 20150101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3Pb9MwFLZggMQF8ZvAqIzEhUOo48R2fGRTJ3ZoFW0glVNkOw6t1CVo6ZD63_Oek0UtQnDh0KqNHdWNn-3v-T1_HyHvYVXPc89NXCV5HWfI9wl-SBoLbWWdKlErUwexCbVY5MulLvakvjAnrKcH7h_cVAueAQJMAIbYTHht4QUYm_HKOZcoi7MvU3rPmQq7K4DTpRrjkjyfXl3iMX3_MRTGKO-9tw4Fuv4_YczfUyX31p6zx-TRABrpp76xT8gd3zwlD3oZyd0z0p43q7UNuVe0renFED0fvp7iwZXKULOxOOV11O7o5ZXZbOi8l8b1HYVZApPT4VOxMt9bt9u23bqjM-SXMG6Ht8wNin1Bqe-ek69nsy-nn-NBSCF2mWbbuAKnopJ1biR0WaJtKq11AAVtZhKPu6BGMVEz4UXFlEqsq7QTlhtWcQaWlqQvyFHTNv4VoYJVBkCNETXGL2VqKpXbNM1UbTI85hqR6e1jLd3AMo5iF5syeBs8L4eOCFFvWXIWkQ_jHT96ho2_1D3BnhrrITd2uAAWUw4WU_7LYiJyfNvP5TBgu5KnWupMZwp-491YDEMN4yem8e1NqAOADRCfiMjL3izGlqQoi55LGRF1YDAHTT0sadarQOcNHivS-L3-H__tDXnIcUMAySjFMTnaXt_4t-S--7ldd9cTclctVXjPJ-TeyWxRXEzCuJlgymsB14rzefHtF5NnHcM |
| linkProvider | Directory of Open Access Journals |
| linkToHtml | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V3Pb9MwFH4aHWhc-D0IDDASHDiEJk4cJweEYGxatbWq2JDGKdiOs1bqktF0oP5T_I28l6TditBuO3CI1NRO5Lqfn9-zn78P4DXO6nFsuXIzP87dkPg-MQ4JXJHoKA-kyKXKa7EJORjEx8fJcA1-L87CUFrlwibWhjorDa2Rd3mQREmYhNL7cPbDJdUo2l1dSGg0sNi3818YslXve5_x_33D-e7O0fae26oKuCZMvJmboYedRXmsImy_n-gg0tqgX6RD5VtaElTSE7knrMg8KX1tssQIzZWXcQ-73Q_wvTdgPSSwd2B92OsPv12s6mB8EMnlfiiPu6eHRA9g39WFLsmKX5r_apmAf_m2f6doXprzdu_-b711D-603jX72AyH-7Bmiwdwq9HbnD-EsleMxrpOUmNlzr60aQbt7Tad8MkUUxNNc0PF9JwdnqrJhPUbDWFbMTSnlMWPn4YjdVKa-aysxhXbISIOZeb0SF-RKhqW2uoRfL2WX7sJnaIs7BNgwssUen9K5LTRGwUqk7EOglDmKqTzwA50FzhITUvHTqogk7QOy3ictsip0wOilHsOvF0-cdZQkVxR9xNBa1mPSMTrL8rpSdrapDQRPMTgykcPX4fCJhovDF89nhljfKkd2FqAK20tW5VeIMuBV8titEm00aQKW57XddCzRddYOPC4wfGyJQHpx8dR5IBcQfhKU1dLivGo5j3H0J74Dp9e3ayXsLF31D9ID3qD_Wdwm9P6CHFzii3ozKbn9jncND9n42r6oh28DL5f9wj4A26Kh3A |
| linkToPdf | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Nb9NAEB2VFCoufBcMBYwEBw4m9trrtQ8IQduIqCSKKEjlZPbLTaTULnEKyl_j1zFjO2mDUG89cIiUeNfWbjw7-2Z39j2AlzirJ4ll0jNBknsR8X1iHBJ6PFVxHgqeC5nXYhNiOEyOjtLRBvxenoWhtMqlT6wdtSk1rZF3WZjGaZRGwu_mbVrEaK_37vSHRwpStNO6lNNoTOTALn5h-Fa97e_hu37FWG__y-5Hr1UY8HSU-nPPINo2cZ7IGPsSpCqMldKIkVQkA0vLg1L4PPe55cYXIlDapJorJn3DfHwFQYjPvQabCMkj1oHNUX8w-na-woOxQixWe6Ms6Z4cElWAfVMXeiQxfmEurCUD_oVz_07XvDD_9W7_z__cHbjVom73fTNM7sKGLe7BjUaHc3Efyn4xnqg6ec0tc_dzm37Q_tylkz9GunKqaM6oXLVwD0_kdOoOGm1hW7noZim7H7-NxvK41It5WU0qd58IOqRe0C0DSWppWGqrB_D1Snq7DZ2iLOwjcLlvJKJCyXPaAI5DaUSiwjASuYzonLAD3aVNZLqlaSe1kGlWh2ssyVorqtMG4oz5Drxe3XHaUJRcUvcDmdmqHpGL1xfK2XHW-qos5SzCoCtA5K8iblOFHwxrfWa01oFQDuwsDS1rPV6VnVuZAy9WxeiraANKFrY8q-sg4kXIzB142Nj0qiUh6conceyAWLP2taaulxSTcc2HjiE_8SA-vrxZz2ELzT771B8ePIGbjJZNiLKT70BnPjuzT-G6_jmfVLNn7Th24ftVD4A_StGQMA |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Inhibition+of+Respiration+of+Candida+albicans+by+Small+Molecules+Increases+Phagocytosis+Efficacy+by+Macrophages&rft.jtitle=mSphere&rft.au=Cui%2C+Shuna&rft.au=Li%2C+Minghui&rft.au=Hassan%2C+Rabeay+Y.+A.&rft.au=Heintz-Buschart%2C+Anna&rft.date=2020-04-15&rft.pub=American+Society+for+Microbiology&rft.eissn=2379-5042&rft.volume=5&rft.issue=2&rft_id=info:doi/10.1128%2FmSphere.00016-20&rft_id=info%3Apmid%2F32295866&rft.externalDocID=PMC7160677 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2379-5042&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2379-5042&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2379-5042&client=summon |