Abstract:
:Cerebral malaria is a complication of Plasmodium falciparum infection characterized by sudden coma, death, or neurodisability. Studies using a mouse model of experimental cerebral malaria (ECM) have indicated that blood-brain barrier disruption and CD8 T cell recruitment contribute to disease, but the spatiotemporal mechanisms are poorly understood. We show by ultra-high-field MRI and multiphoton microscopy that the olfactory bulb is physically and functionally damaged (loss of smell) by Plasmodium parasites during ECM. The trabecular small capillaries comprising the olfactory bulb show parasite accumulation and cell occlusion followed by microbleeding, events associated with high fever and cytokine storm. Specifically, the olfactory upregulates chemokine CCL21, and loss or functional blockade of its receptors CCR7 and CXCR3 results in decreased CD8 T cell activation and recruitment, respectively, as well as prolonged survival. Thus, early detection of olfaction loss and blockade of pathological cell recruitment may offer potential therapeutic strategies for ECM.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Zhao H,Aoshi T,Kawai S,Mori Y,Konishi A,Ozkan M,Fujita Y,Haseda Y,Shimizu M,Kohyama M,Kobiyama K,Eto K,Nabekura J,Horii T,Ishino T,Yuda M,Hemmi H,Kaisho T,Akira S,Kinoshita M,Tohyama K,Yoshioka Y,Ishii KJ,Codoi
10.1016/j.chom.2014.04.008subject
Has Abstractpub_date
2014-05-14 00:00:00pages
551-63issue
5eissn
1931-3128issn
1934-6069pii
S1931-3128(14)00142-5journal_volume
15pub_type
杂志文章abstract::Intracellular nucleotide-binding leucine-rich repeat (NLR) receptors play central roles in human and plant innate immunity. In this issue of Cell Host & Microbe, Wang et al. (2015) show that a single plant NLR can detect diverse pathogen effectors by partnering with different scaffolding proteins, which can each recog...
journal_title:Cell host & microbe
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abstract::The HIV-1 accessory protein Vpr enhances infection of primary macrophages through unknown mechanisms. Recent studies demonstrated that Vpr interactions with the cellular DCAF1-DDB1-CUL4 E3 ubiquitin ligase complex limit activation of innate immunity and interferon (IFN) induction. We describe a restriction mechanism t...
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journal_title:Cell host & microbe
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journal_title:Cell host & microbe
pub_type: 杂志文章
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journal_title:Cell host & microbe
pub_type: 杂志文章
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journal_title:Cell host & microbe
pub_type: 杂志文章
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abstract::It is currently unclear at which point during viral replication that RNA genomes are first recognized as nonself by the immune system. In this issue of Cell Host & Microbe, Weber et al. show that incoming nucleocapsid-bound genomes are sufficient to bind and activate innate immune sensors. ...
journal_title:Cell host & microbe
pub_type: 评论,杂志文章
doi:10.1016/j.chom.2013.02.012
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journal_title:Cell host & microbe
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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journal_title:Cell host & microbe
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journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2019.10.013
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2018.03.019
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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更新日期:2019-02-13 00:00:00
abstract::The emergence of circulating vaccine-derived polioviruses through evolution of the oral polio vaccine (OPV) poses a significant obstacle to polio eradication. Understanding the early genetic changes that occur as OPV evolves and transmits is important for preventing future outbreaks. Here, we use deep sequencing to de...
journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2020.10.011
更新日期:2021-01-13 00:00:00
abstract::The intestinal microbiota is important for induction of inflammatory bowel disease (IBD). IBD is associated with complex shifts in microbiota composition, but it is unclear whether specific bacterial subsets induce IBD and, if so, whether their proportions in the microbiota are altered during disease. Here, we fulfill...
journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2011.04.009
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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journal_title:Cell host & microbe
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journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2016.01.004
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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journal_title:Cell host & microbe
pub_type: 杂志文章
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journal_title:Cell host & microbe
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journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2009.12.002
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
doi:10.1016/j.chom.2008.11.006
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journal_title:Cell host & microbe
pub_type: 评论,杂志文章
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journal_title:Cell host & microbe
pub_type: 杂志文章
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journal_title:Cell host & microbe
pub_type: 杂志文章
doi:10.1016/j.chom.2019.09.008
更新日期:2019-10-09 00:00:00
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journal_title:Cell host & microbe
pub_type: 杂志文章
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