• Corpus ID: 83977536

Complementary immune roles for infected and uninfected cells during Legionella pneumophila infection

  title={Complementary immune roles for infected and uninfected cells during Legionella pneumophila infection},
  author={Alan M Copenhaver},
The innate immune system responds to virulent pathogens, yet many pathogens manipulate host-signaling pathways, which should limit immune activation. The intracellular bacterium Legionella pneumophila is the cause of the severe pneumonia Legionnaire's disease. L. pneumophila encodes a type IV secretion system (T4SS) to translocate bacterial proteins into the cytosol of infected host cells. Several of these bacterial effectors (Lgt1, Lgt2, Lgt3, SidI, SidL, Pkn5, and Lpg1489) inactivate host… 


Innate Immunity to Intracellular Pathogens: Lessons Learned from Legionella pneumophila.
  • Sunny Shin
  • Biology, Medicine
    Advances in applied microbiology
  • 2012
This chapter discusses a few examples demonstrating how the study of immune responses triggered specifically by the L. pneumophila type IV secretion system has provided unique insight into the understanding of host immunity against intracellular bacterial pathogens.
The Frustrated Host Response to Legionella pneumophila Is Bypassed by MyD88-Dependent Translation of Pro-inflammatory Cytokines
A perspective of how host cells are able to cope with pathogen-encoded activities that disrupt normal cellular process and initiate a successful inflammatory response is offered.
Host cell processes that influence the intracellular survival of Legionella pneumophila
This review discusses how L. pneumophila manipulates host cells, as well as host cell processes that either facilitate or impede its intracellular survival.
Secreted Bacterial Effectors That Inhibit Host Protein Synthesis Are Critical for Induction of the Innate Immune Response to Virulent Legionella pneumophila
These results provide a striking illustration of how the host immune response to a virulent pathogen can also be shaped by pathogen-encoded activities, such as inhibition of host protein synthesis.
Alveolar Macrophages and Neutrophils Are the Primary Reservoirs for Legionella pneumophila and Mediate Cytosolic Surveillance of Type IV Secretion
The data suggest that alveolar macrophages and neutrophils are both an intracellular reservoir for L. pneumophila and a source of proinflammatory cytokines that contribute to the host immune response against L.neumophila.
Identification of Host Cytosolic Sensors and Bacterial Factors Regulating the Type I Interferon Response to Legionella pneumophila
The results provide new insights into the molecular mechanisms by which an intracellular bacterial pathogen activates and also represses innate immune responses and a secreted effector protein, SdhA, is identified as a key suppressor of the IFN response to L. pneumophila.
Activation of Host Mitogen-Activated Protein Kinases by Secreted Legionella pneumophila Effectors That Inhibit Host Protein Translation
The results demonstrate that this important host pathway can be activated in response to a pathogen-encoded activity, adding to an emerging body of evidence in support of this novel mode of innate immune detection in metazoans.
Modulation of host cell function by Legionella pneumophila type IV effectors.
This review focuses on intracellular trafficking of L. pneumophila and describes how bacterial proteins contribute to modulation of host processes required for survival within host cells.
Type IV Secretion-Dependent Activation of Host MAP Kinases Induces an Increased Proinflammatory Cytokine Response to Legionella pneumophila
A previously uncharacterized host response to bacterial type IV secretion that activates MAPK signaling is defined and coincident detection of multiple bacterial components enables immune discrimination between virulent and avirulent bacteria.
Legionella pneumophila pathogenesis and immunity.
New findings are described that demonstrate that various cytokines that define Th1 vs Th2 helper cell activity also are important in regulating resistance versus susceptibility to this ubiquitous microorganism.