Microglia and amyloid precursor protein coordinate control of transient Candida cerebritis with memory deficits View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Yifan Wu, Shuqi Du, Jennifer L. Johnson, Hui-Ying Tung, Cameron T. Landers, Yuwei Liu, Brittany G. Seman, Robert T. Wheeler, Mauro Costa-Mattioli, Farrah Kheradmand, Hui Zheng, David B. Corry

ABSTRACT

Bloodborne infections with Candida albicans are an increasingly recognized complication of modern medicine. Here, we present a mouse model of low-grade candidemia to determine the effect of disseminated infection on cerebral function and relevant immune determinants. We show that intravenous injection of 25,000 C. albicans cells causes a highly localized cerebritis marked by the accumulation of activated microglial and astroglial cells around yeast aggregates, forming fungal-induced glial granulomas. Amyloid precursor protein accumulates within the periphery of these granulomas, while cleaved amyloid beta (Aβ) peptides accumulate around the yeast cells. CNS-localized C. albicans further activate the transcription factor NF-κB and induce production of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor (TNF), and Aβ peptides enhance both phagocytic and antifungal activity from BV-2 cells. Mice infected with C. albicans display mild memory impairment that resolves with fungal clearance. Our results warrant additional studies to understand the effect of chronic cerebritis on cognitive and immune function. More... »

PAGES

58

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-018-07991-4

DOI

http://dx.doi.org/10.1038/s41467-018-07991-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1111014672

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30610193


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