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A Subpopulation of Intracellular Neisseria gonorrhoeae Escapes Autophagy-Mediated Killing Inside Epithelial Cells.

Identifieur interne : 000402 ( Main/Exploration ); précédent : 000401; suivant : 000403

A Subpopulation of Intracellular Neisseria gonorrhoeae Escapes Autophagy-Mediated Killing Inside Epithelial Cells.

Auteurs : Ping Lu [République populaire de Chine] ; Shuyi Wang [République populaire de Chine] ; Yan Lu [République populaire de Chine] ; Dante Neculai [République populaire de Chine] ; Qiming Sun [République populaire de Chine] ; Stijn Van Der Veen [République populaire de Chine]

Source :

RBID : pubmed:29688440

Descripteurs français

English descriptors

Abstract

The bacterial pathogen Neisseria gonorrhoeae is able to transmigrate across the mucosal epithelia following the intracellular route and cause disseminated infections. It is currently unknown whether the autophagy pathway is able target intracellular N. gonorrhoeae for destruction in autolysosomes or whether this bacterium is able to escape autophagy-mediated killing. In this study, we demonstrate that during the early stage of epithelial cell invasion, N. gonorrhoeae is targeted by the autophagy pathway and sequestered into double-membrane autophagosomes that subsequently fuse with lysosomes for destruction. However, a subpopulation of the intracellular gonococci is able to escape early autophagy-mediated killing. N. gonorrhoeae is subsequently able to inhibit this pathway, allowing intracellular survival and exocytosis. During this stage, N. gonorrhoeae activates the autophagy repressor mammalian target of rapamycin complex 1 and inhibits autophagosome maturation and lysosome fusion. Thus, our results provide novel insight into the interactions between N. gonorrhoeae and the autophagy pathway during invasion and transcytosis of epithelial cells.

DOI: 10.1093/infdis/jiy237
PubMed: 29688440


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">The bacterial pathogen Neisseria gonorrhoeae is able to transmigrate across the mucosal epithelia following the intracellular route and cause disseminated infections. It is currently unknown whether the autophagy pathway is able target intracellular N. gonorrhoeae for destruction in autolysosomes or whether this bacterium is able to escape autophagy-mediated killing. In this study, we demonstrate that during the early stage of epithelial cell invasion, N. gonorrhoeae is targeted by the autophagy pathway and sequestered into double-membrane autophagosomes that subsequently fuse with lysosomes for destruction. However, a subpopulation of the intracellular gonococci is able to escape early autophagy-mediated killing. N. gonorrhoeae is subsequently able to inhibit this pathway, allowing intracellular survival and exocytosis. During this stage, N. gonorrhoeae activates the autophagy repressor mammalian target of rapamycin complex 1 and inhibits autophagosome maturation and lysosome fusion. Thus, our results provide novel insight into the interactions between N. gonorrhoeae and the autophagy pathway during invasion and transcytosis of epithelial cells.</div>
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<name sortKey="Lu, Ping" sort="Lu, Ping" uniqKey="Lu P" first="Ping" last="Lu">Ping Lu</name>
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<name sortKey="Lu, Yan" sort="Lu, Yan" uniqKey="Lu Y" first="Yan" last="Lu">Yan Lu</name>
<name sortKey="Neculai, Dante" sort="Neculai, Dante" uniqKey="Neculai D" first="Dante" last="Neculai">Dante Neculai</name>
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