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Published on: November 22, 2013
Legionella and mitochondria, an intriguing relationship
Francisco Javier García-Rodríguez1, Carmen Buchrieser1, Pedro Escoll1
1Institut Pasteur, Université Paris Cité, Biologie des Bactéries Intracellulaires and CNRS UMR 6047, Paris, France.
Abstract:
Legionella pneumophila is the causative agent of Legionnaires' disease, a severe pneumonia. L. pneumophila injects via a type-IV-secretion-system (T4SS) more than 300 bacterial proteins into macrophages, its main host cell in humans. Certain of these bacterial effectors target organelles in the infected cell and hijack multiple processes to facilitate all steps of the intracellular life cycle of this pathogen. In this review, we discuss the interplay between L. pneumophila, an intracellular bacterium fully armed with virulence tools, and mitochondria, the extraordinary eukaryotic organelles playing prominent roles in cellular bioenergetics, cell-autonomous immunity and cell death. We present and discuss key findings concerning the multiple interactions of L. pneumophila with mitochondria during infection and the mechanisms employed by T4SS effectors that target mitochondrial functions to subvert infected cells.
Insights
Legionella pneumophila causes Legionnaires' disease by injecting effector proteins into human macrophages. This review details how these bacterial proteins target mitochondria, crucial organelles involved in energy, immunity, and cell death, to aid pathogen survival.
Area of Science:
- Microbiology
- Cell Biology
- Pathogenesis
Background:
- Legionella pneumophila is the primary cause of Legionnaires' disease, a severe form of pneumonia.
- This intracellular bacterium infects human macrophages, utilizing a type-IV-secretion-system (T4SS) to deliver over 300 effector proteins.
- These effectors manipulate host cell processes and organelles to facilitate the pathogen's intracellular lifecycle.
Approach:
- This review synthesizes current research on the interactions between L. pneumophila and host cell mitochondria.
- It focuses on the mechanisms by which T4SS effectors target mitochondrial functions.
- The discussion covers mitochondria's roles in cellular bioenergetics, immunity, and cell death during infection.
Key Points:
- L. pneumophila extensively interacts with mitochondria, a central organelle in cellular energy production and immune responses.
- T4SS effectors are key virulence factors that actively subvert mitochondrial functions.
- These targeted manipulations aid the bacterium in establishing and maintaining intracellular infection.
Conclusions:
- Mitochondria are critical targets for L. pneumophila virulence strategies.
- Understanding these interactions provides insights into host-pathogen dynamics and potential therapeutic targets.
- The hijacking of mitochondrial functions is essential for L. pneumophila's intracellular survival and pathogenesis.
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