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2. Role of astrocyte senescence regulated by the non– canonical autophagy in the neuroinflammation associated to cerebral malaria

Author

Hellani, Fatima, primary, Leleu, Inès, additional, Saidi, Nasreddine, additional, Martin, Nathalie, additional, Lecoeur, Cécile, additional, Werkmeister, Elisabeth, additional, Koffi, David, additional, Trottein, François, additional, Yapo-Etté, Hélène, additional, Das, Bidyut, additional, Abbadie, Corinne, additional, and Pied, Sylviane, additional

Published
2023
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5. Role of astrocyte senescence induced by Plasmodium in the pathogenesis of Cerebral Malaria

Author

Hellani, Fatima, Saidi, Nasreddine, Leleu, Inès, Roland, Jacques, Martin, Nathalie, Abaddie, Corinne, Pied, Sylviane, and Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, [SDV]Life Sciences [q-bio], parasitic diseases, [SDV.IMM]Life Sciences [q-bio]/Immunology
Abstract

International audience; Cerebral malaria (CM) is a fatal neurological syndrom due to Plasmodium (P.) falciparum infection, which kills 405,000 people annually(1). A central event involved in the pathogenesis of CM is the sequestration of infected red blood cells in the brain capillaries and the inflammatory response of activated glial cells (2). However, molecular mechanisms involved in the induction of the pro-inflammatory response of glial cells during CM remains unknown. In this study, we have examined if the senescence of glial cells induced by P. berghei ANKA infection participates in the neuroinflammatory response associated to CM.

Published
2021

6. A non canonical autophagy is involved in the transfer of Plasmodium microvesicles to astrocytes

Author

Leleu, Inès, Delcroix-Genete, Delphine, Salome-Desnoulez, Sophie, Saidi, Nasreddine, Brodin, Priscille, Lafont, Frank, Tomavo, Stanislas, Pied, Sylviane, and Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV]Life Sciences [q-bio]
Abstract

International audience; Cerebralmalaria(CM)isaninflammatorydisease,inducedinHumanbyPlasmodium(P.)falciparumprotozoanparasite,causingeachyearalmostof445000deathsinendemicareas.Theneuropathophysiologyistheresultofthesequestrationofinfectedredbloodcellsincerebralmicrovesselsandtheactivationofastrocytes.Thispromotesanexacerbatedinflammatoryresponsecharacterizedbyahighproductionofpro-inflammatorycytokinesandchemokinesandthebraininfiltrationbypathologicTCD8+lymphocytes1,2,3.Astrocytesaremajorbraincellswhichplayimportantrolesinthehomeostasisofthecentralnervoussystemaswellastheintegrityofthebrainbloodbarrierandthelocalinnateimmuneresponse4.InthemodelofP.bergheiANKA(PbA),wehavepreviouslyshownatransferofparasiticmicrovesicles(PbA-MVs)toastrocytes4.Inthisstudy,usingtheexperimentalcerebralmalariamodel(ECM)ofsusceptibleC57BL/6(CMS)miceinfectedwithPbA,mimickinginpartthehumandisease,weshowthatanunconventionalLC3-mediatedautophagypathwaycalledLC3-associatedphagocytosis(LAP)isinvolvedinthetransferofPbA-MVstoprimaryastrocytesculturesuponcontactwithPbA-infectedredbloodcells(PbA-iRBCs),whicharethenintracellularlydegraded5.WealsoshownthataBafilomycinA1(BAFA1),aninhibitorofautophagy,treatmentofCMSmicepreventsECM.Theseresultswereconfirmedbythepretreatmentofprimaryastrocyteculturewith3-Methyladenine,anotherautophagyinhibitor,whichblocksthePbA-MVsattheplasmaticmembraneofastrocytes.Intersingly,wealsoshownthattheLAPinastrocyteswasassociatedwiththeproductionofpro-inflammatoryCXCL-10,CCL-2andTNF-α.Altogether,ourdatashownthatAstrocyteisanimportantplayerintheneuroinflammatoryprocessofCMandmaybeanimmunotherapeutictarget.

Published
2021

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