دورية أكاديمية
Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection.
| العنوان: | Chlamydia trachomatis induces disassembly of the primary cilium to promote the intracellular infection. |
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| المؤلفون: | Ekka, Roseleen, Gutierrez, Abraham, Johnson, Kirsten A., Tan, Ming, Sütterlin, Christine |
| المصدر: | PLoS Pathogens; 6/17/2024, Vol. 20 Issue 6, p1-22, 22p |
| مصطلحات موضوعية: | CHLAMYDIA trachomatis, CILIA & ciliary motion, CHLAMYDIA infections, CELL physiology, CELL anatomy, CELL culture |
| مستخلص: | Chlamydia trachomatis is a clinically important bacterium that infects epithelial cells of the genitourinary and respiratory tracts and the eye. These differentiated cells are in a quiescent growth state and have a surface organelle called a primary cilium, but the standard Chlamydia cell culture infection model uses cycling cells that lack primary cilia. To investigate if these differences are relevant, we performed infections with host cells that have a primary cilium. We found that C. trachomatis caused progressive loss of the primary cilium that was prevented by disrupting Aurora A (AurA), HDAC6 or calmodulin, which are components of the cellular cilia disassembly pathway. Stabilization of the primary cilium by targeting this pathway caused a large reduction in infectious progeny although there were no changes in chlamydial inclusion growth, chlamydial replication or the ultrastructural appearance of dividing and infectious forms (RBs and EBs, respectively). Thus, the presence of a primary cilium interfered with the production of infectious EBs at a late step in the developmental cycle. C. trachomatis infection also induced quiescent cells to re-enter the cell cycle, as detected by EdU incorporation in S-phase, and Chlamydia-induced cilia disassembly was necessary for cell cycle re-entry. This study therefore describes a novel host-pathogen interaction in which the primary cilium limits a productive Chlamydia infection, and the bacterium counteracts this host cell defense by activating the cellular cilia disassembly pathway. Author summary: In this study, we describe a novel tussle between the pathogenic bacterium Chlamydia trachomatis and its infected host cell. This interaction is centered on the primary cilium, which is a protrusion on the cell surface that is important for many cellular functions. While the primary cilium is present on cells infected by Chlamydia during a natural infection, it is absent from dividing cells used to study Chlamydia infections in cell culture. We found that Chlamydia infection caused loss of the primary cilium by activating the cellular cilia disassembly machinery and induced a quiescent host cell to re-enter the cell cycle. Furthermore, we showed that the presence of a primary cilium severely inhibited the production of infectious chlamydial progeny. Thus, the host cell uses the primary cilium to restrict a productive infection, while Chlamydia induces cilia disassembly as a countermeasure. This host-pathogen interaction could be unique to Chlamydia, but it could also have been missed for other intracellular bacteria and viruses, which are commonly studied in cells that lack a primary cilium. This work could lead to new antimicrobial approaches targeting the primary cilium. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: | Complementary Index |
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