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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

. 2023 ; 42 (10) : 113240. [pub] 20231017

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S.

Perzistentní odkaz   https://www.medvik.cz/link/bmc24000959

Grantová podpora
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

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.

Citace poskytuje Crossref.org

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$a The fungal pathogen Candida albicans is linked to chronic brain diseases such as Alzheimer's disease (AD), but the molecular basis of brain anti-Candida immunity remains unknown. We show that C. albicans enters the mouse brain from the blood and induces two neuroimmune sensing mechanisms involving secreted aspartic proteinases (Saps) and candidalysin. Saps disrupt tight junction proteins of the blood-brain barrier (BBB) to permit fungal brain invasion. Saps also hydrolyze amyloid precursor protein (APP) into amyloid β (Aβ)-like peptides that bind to Toll-like receptor 4 (TLR4) and promote fungal killing in vitro while candidalysin engages the integrin CD11b (Mac-1) on microglia. Recognition of Aβ-like peptides and candidalysin promotes fungal clearance from the brain, and disruption of candidalysin recognition through CD11b markedly prolongs C. albicans cerebral mycosis. Thus, C. albicans is cleared from the brain through innate immune mechanisms involving Saps, Aβ, candidalysin, and CD11b.
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$a Corry, David B $u Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Departments of Pathology & Immunology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Biology of Inflammation Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Michael E. DeBakey VA Center for Translational Research on Inflammatory Diseases, Houston, TX 77030, USA. Electronic address: dcorry@bcm.edu
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