Amoeba host‐ L egionella synchronization of amino acid auxotrophy and its role in bacterial adaptation and pathogenic evolution

• Published in: Environmental microbiology Vol. 16; no. 2; pp. 350 - 358
• Main Authors: Price, Christopher T. D., Richards, Ashley M., Von Dwingelo, Juanita E., Samara, Hala A., Abu Kwaik, Yousef
• Format: Journal Article
• Language: English
• Published: 01-02-2014
• ISSN: 1462-2912; 1462-2920
• DOI: 10.1111/1462-2920.12290

Summary
L
egionella pneumophila
, the causative agent of
L
egionnaires' disease, invades and proliferates within a diverse range of free‐living amoeba in the environment, but upon transmission to humans, the bacteria hijack alveolar macrophages. Intracellular proliferation of
L
. pneumophila
in two evolutionarily distant hosts is facilitated by bacterial exploitation of conserved host processes that are targeted by bacterial protein effectors injected into the host cell. A key aspect of microbe–host interaction is microbial extraction of nutrients from the host, but understanding of this is still limited.
AnkB
functions as a nutritional virulence factor and promotes host proteasomal degradation of polyubiquitinated proteins generating gratuitous levels of limiting host cellular amino acids.
L
egionella pneumophila
is auxotrophic for several amino acids including cysteine, which is a metabolically preferred source of carbon and energy during intracellular proliferation, but is limiting in both amoebae and humans. We propose that synchronization of bacterial amino acids auxotrophy with the host is a driving force in pathogenic evolution and nutritional adaptation of
L
. pneumophila
and other intracellular bacteria to life within the host cell. Understanding microbial strategies of nutrient generation and acquisition in the host will provide novel antimicrobial strategies to disrupt pathogen access to essential sources of carbon and energy.