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Amoeba host‐ L egionella synchronization of amino acid auxotrophy and its role in bacterial adaptation and pathogenic evolution
Author(s) -
Price Christopher T. D.,
Richards Ashley M.,
Von Dwingelo Juanita E.,
Samara Hala A.,
Abu Kwaik Yousef
Publication year - 2014
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.12290
Subject(s) - biology , legionella pneumophila , microbiology and biotechnology , virulence , host (biology) , auxotrophy , intracellular parasite , bacteria , amino acid , intracellular , effector , host–pathogen interaction , gene , biochemistry , genetics , mutant
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.