Programmed cell death in Legionella infection
Details
Publication Year 2014-01, Volume 9, Issue #1, Page 107-118
Journal Title
Future Microbiology
Publication Type
Journal Article
Abstract
The causative agent of Legionnaires' disease, Legionella pneumophila, resides within alveolar macrophages by exporting 295 bacterial virulence proteins (effectors) to modulate host cell processes. This leads to the formation of a unique vacuolar niche and the suppression of macrophage cell death pathways, which, in turn, promote bacterial survival and allow sufficient time for replication. However, once nutrients within the vacuole are depleted, Legionella must act to induce host cell death in order to facilitate bacterial egress and reinfect new cells. Intracellular Legionella also evade detection by the host cell's innate immune system, which seeks to destroy invading pathogens by activating inflammasome complexes, thereby promoting proinflammatory cytokine activation and pyroptotic cell death. Understanding how different forms of programmed cell death contribute to Legionella infectivity and are manipulated by Legionella effector proteins will be important for identifying novel antibacterial therapeutic targets.
Publisher
Future Medicine
WEHI Research Division(s)
Inflammation
Rights Notice
Refer to copyright notice on published article.


Creation Date: 2014-06-19 12:07:53
Last Modified: 0001-01-01 12:00:00
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