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Toll-like receptor 4 and CD11b expressed on microglia coordinate eradication of Candida albicans cerebral mycosis
Y. Wu, S. Du, LH. Bimler, KE. Mauk, L. Lortal, N. Kichik, JS. Griffiths, R. Osicka, L. Song, K. Polsky, L. Kasper, P. Sebo, J. Weatherhead, JM. Knight, F. Kheradmand, H. Zheng, JP. Richardson, B. Hube, JR. Naglik, DB. Corry
Language English Country United States
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.
Grant support
R01 HL140398
NHLBI NIH HHS - United States
R41 AI164997
NIAID NIH HHS - United States
T32 HL139425
NHLBI NIH HHS - United States
Wellcome Trust - United Kingdom
K08 AI143968
NIAID NIH HHS - United States
T32 HL007747
NHLBI NIH HHS - United States
R37 DE022550
NIDCR NIH HHS - United States
I01 BX004828
BLRD VA - United States
P30 CA125123
NCI NIH HHS - United States
T32 AI053831
NIAID NIH HHS - United States
R01 HL117181
NHLBI NIH HHS - United States
R01 AI135803
NIAID NIH HHS - United States
S10 RR024574
NCRR NIH HHS - United States
214229_Z_18_Z
Wellcome Trust - United Kingdom
NLK
Cell Press Free Archives
from 2012
Directory of Open Access Journals
from 2012
Free Medical Journals
from 2012
Freely Accessible Science Journals
from 2012-01-26
Open Access Digital Library
from 2012-01-01
Open Access Digital Library
from 2012-01-26
- MeSH
- Alzheimer Disease metabolism microbiology MeSH
- Amyloid beta-Peptides metabolism MeSH
- CD11b Antigen * metabolism MeSH
- Candida albicans metabolism MeSH
- Fungal Proteins metabolism MeSH
- Microglia * metabolism microbiology MeSH
- Mycoses * genetics metabolism MeSH
- Mice MeSH
- Toll-Like Receptor 4 * metabolism MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
The fungal pathogen Candida albicans is linked to chronic brain diseases such as Alzheimer's disease (AD), but the molecular basis of brain anti-Candida immunity remains unknown. We show that C. albicans enters the mouse brain from the blood and induces two neuroimmune sensing mechanisms involving secreted aspartic proteinases (Saps) and candidalysin. Saps disrupt tight junction proteins of the blood-brain barrier (BBB) to permit fungal brain invasion. Saps also hydrolyze amyloid precursor protein (APP) into amyloid β (Aβ)-like peptides that bind to Toll-like receptor 4 (TLR4) and promote fungal killing in vitro while candidalysin engages the integrin CD11b (Mac-1) on microglia. Recognition of Aβ-like peptides and candidalysin promotes fungal clearance from the brain, and disruption of candidalysin recognition through CD11b markedly prolongs C. albicans cerebral mycosis. Thus, C. albicans is cleared from the brain through innate immune mechanisms involving Saps, Aβ, candidalysin, and CD11b.
Biology of Inflammation Center Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA
Department of Medicine Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA
Department of Neuroscience Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA
Department of Pediatrics Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA
Huffington Center on Aging Baylor College of Medicine One Baylor Plaza Houston TX 77030 USA
Institute of Microbiology Friedrich Schiller University 07737 Jena Germany
Institute of Microbiology of the Czech Academy of Sciences Prague Czech Republic
Michael E DeBakey VA Center for Translational Research on Inflammatory Diseases Houston TX 77030 USA
References provided by Crossref.org
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