Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 120, Issue 5, Pages 1389-1392Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI42949
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL059842] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI033774, R01AI052733, R37AI033142, R01AI033142] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL059842, HL059842] Funding Source: Medline
- NIAID NIH HHS [AI033142, AI052733, R37 AI033142, R01 AI033142, AI033774, R01 AI052733, R01 AI033774] Funding Source: Medline
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The mechanism by which Cryptococcus neoformans invades the central nervous system is fundamental for understanding pathogenesis because cryptococcosis commonly presents as meningoencephalitis. There is evidence for both direct invasion of the endothelial cells lining the brain vasculature and a Trojan horse mechanism whereby cryptococci enter the central nervous system after macrophage ingestion. However, in this issue of the JCI, Shi et al. use intravital microscopy to reveal that brain invasion by C neoformans follows a capillary microembolic event. They find that after suddenly stopping in brain capillaries, cryptococci cross into the central nervous system in a process that is urease dependent, requires viability, and involves cellular deformation. This observation provides evidence for direct brain invasion by C. neoformans, but a consideration of all the currently available evidence suggests a role for both direct and phagocyte-associated invasion. Hence, the remarkable neurotropism of C. neoformans may have more than one mechanism.
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