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X-WR-RELCALID:www_embl_org_seminar_13380.ics
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DTSTAMP:20210421T204154Z
LOCATION:Virtual Seminar\, EMBL Barcelona\, C/ Dr. Aiguader\, 88\, PRBB Bui
 lding\, 08003 Barcelona\, Spain
SUMMARY;LANGUAGE=en-us:Marina  de Niz: Breaking and entering: imaging-based 
 findings of the voyage of Trypanosoma brucei into host tissues.
DESCRIPTION:EMBL Barcelona Postdoc Seminar Series\nSpeaker: Marina  de Niz\
 nInstitution: iMM Lisboa\, Portugal\nHost: Maria Bernabeu\nAbstract: Trypa
 nosoma brucei is responsible for lethal diseases in humans and cattle in S
 ub-Saharan Africa. These extracellular parasites extravasate from the bloo
 d circulation into several tissues. The importance of the vasculature in t
 issue tropism is poorly understood\, as is the microenvironment that each 
 organ provides for parasite replication and differentiation. Using intravi
 tal imaging and bioluminescence\, we found that gonadal white adipose tiss
 ue and pancreas are the two main parasite reservoirs. We show that reservo
 ir establishment happens before vascular permeability is compromised\, sug
 gesting that extravasation is an active mechanism. Blocking endothelial su
 rface adhesion molecules (E-selectin\, P-selectins\, or ICAM2) significant
 ly reduced extravascular parasite load in all organs and delayed host leth
 ality. Remarkably\, blocking CD36 had a specific effect on adipose tissue 
 tropism that was sufficient to delay lethality\, suggesting that establish
 ment of the adipose tissue reservoir is necessary for parasite virulence. 
 This works demonstrates the importance of the vasculature in a T. brucei i
 nfection and identifies organ-specific adhesion molecules as key players f
 or tissue tropism. Furthermore\, we found that specific organs such as the 
 spleen\, adipose tissue and pancreas provide important microenvironment fo
 r the development\, replication and differentiation of T. brucei during it
 s life cycle within the mammalian host. \n
DTSTART:20210413T123000Z
LAST-MODIFIED:20210421T204154Z
DURATION:PT1H
UID:www.embl.org/13380
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