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Legionella longbeachae Is Immunologically Silent and Highly Virulent In Vivo
Liliana M Massis1, Mariana A Assis-Marques1, Fernanda V S Castanheira2
1Department of Cell Biology.
Background:
Legionella longbeachae (Llo) and Legionella pneumophila (Lpn) are the most common pneumonia-causing agents of the genus. Although both species can be lethal to humans and are highly prevalent, little is known about the molecular pathogenesis of Llo infections. In murine models of infection, Lpn infection is self-limited, whereas Llo infection is lethal.
Methods:
We used mouse macrophages, human macrophages, human epithelial cells, and mouse infections in vivo to evaluate multiple parameters of the infection.
Results:
We determined that the Llo Dot/Icm secretion system is critical for virulence. Different than Lpn, Llo disseminates and the animals develop a severe pulmonary failure, as demonstrated by lung mechanics and blood oxygenation assays. As compared to Lpn, Llo is immunologically silent and fails to trigger the production of cytokines in human pulmonary epithelial cells and in mouse and human macrophages. Infections in Tnfr1-/-, Ifng-/-, and Il12p40-/- mice supported the participation of cytokines for the resistance phenotype.
Conclusions:
Both Lpn and Llo require the Dot/Icm system for pathogenesis, but the infection outcome is strikingly different. Llo is immunologically silent, highly virulent, and lethal. The differences reported herein may reflect unappreciated clinical differences in patients infected with Lpn or Llo.
Insights
Legionella longbeachae (Llo) causes lethal pneumonia by disseminating and evading immune responses, unlike Legionella pneumophila (Lpn). Understanding Llo pathogenesis is crucial for distinguishing clinical outcomes.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Legionella longbeachae (Llo) and Legionella pneumophila (Lpn) are leading causes of Legionnaires' disease pneumonia.
- Llo pathogenesis remains poorly understood, despite its high prevalence and lethality.
- Murine models show Llo infection is lethal, while Lpn infection is self-limiting.
Purpose of the Study:
- To investigate the molecular mechanisms underlying Llo virulence.
- To compare the pathogenesis of Llo and Lpn infections.
- To identify host immune responses involved in resistance to Legionella.
Main Methods:
- Utilized mouse and human macrophages, human epithelial cells, and in vivo murine infection models.
- Assessed pulmonary failure using lung mechanics and blood oxygenation assays.
- Analyzed cytokine production and host immune responses in knockout mouse models (Tnfr1-/-, Ifng-/-, Il12p40-/-).
Main Results:
- The Llo Dot/Icm secretion system is essential for virulence.
- Llo disseminates within the host, leading to severe pulmonary failure.
- Llo is immunologically silent, failing to induce cytokine production, unlike Lpn.
Conclusions:
- Both Lpn and Llo depend on the Dot/Icm system for pathogenesis.
- Llo exhibits high virulence, immunological silence, and lethality.
- Distinct pathogenic mechanisms of Llo and Lpn may explain differing clinical presentations.
