Open AccessThe cellular ceramide transport protein CERT promotes Chlamydia psittaci infection and controls bacterial sphingolipid uptake
Author(s) -
KochEdelmann Sophia,
Banhart Sebastian,
Saied Essa M.,
Rose Laura,
Aeberhard Lukas,
Laue Michael,
Doellinger Joerg,
Arenz Christoph,
Heuer Dagmar
Publication year - 2017
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12752
Subject(s) - biology , sphingolipid , chlamydia psittaci , intracellular parasite , microbiology and biotechnology , ceramide , obligate , chlamydia , genetics , intracellular , apoptosis , ecology
Chlamydiaceae are bacterial pathogens that cause diverse diseases in humans and animals. Despite their broad host and tissue tropism, all Chlamydia species share an obligate intracellular cycle of development and have evolved sophisticated mechanisms to interact with their eukaryotic host cells. Here, we have analysed interactions of the zoonotic pathogen Chlamydia psittaci with a human epithelial cell line. We found that C. psittaci recruits the ceramide transport protein (CERT) to its inclusion. Chemical inhibition and CRISPR/Cas9‐mediated knockout of CERT showed that CERT is a crucial factor for C. psittaci infections thereby affecting different stages of the infection including inclusion growth and infectious progeny formation. Interestingly, the uptake of fluorescently labelled sphingolipids in bacteria inside the inclusion was accelerated in CERT‐knockout cells indicating that C. psittaci can exploit CERT‐independent sphingolipid uptake pathways. Moreover, the CERT‐specific inhibitor HPA‐12 strongly diminished sphingolipid transport to inclusions of infected CERT‐knockout cells, suggesting that other HPA‐12‐sensitive factors are involved in sphingolipid trafficking to C. psittaci . Further analysis is required to decipher these interactions and to understand their contributions to bacterial development, host range, tissue tropism, and disease outcome.