Lipids and Legionella Virulence
The intracellular lung pathogen Legionella pneumophila has developed virulence mechanisms which allow it to replicate in its natural host protozoa as well as in human macrophages. L. pneumophila belongs to the γ-proteobacteria and has several lipid compon
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N. Timmis (ed.), Handbook of Hydrocarbon and Lipid Microbiology, DOI 10.1007/978-3-540-77587-4_242, # Springer-Verlag Berlin Heidelberg, 2010
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Lipids and Legionella Virulence
Abstract: The intracellular lung pathogen Legionella pneumophila has developed virulence mechanisms which allow it to replicate in its natural host protozoa as well as in human macrophages. L. pneumophila belongs to the g-proteobacteria and has several lipid components in its membrane which are not usual in this bacterial group. Membrane phospholipids are substituted with branched chain fatty acyl residues and phosphatidylcholine is a major phospholipid in Legionella. Legionella phosphatidylcholine is an important virulence determinant and acts through multiple mechanisms. Lipopolysaccharides from L. pneumophila show several unusual features among them the substitution with very-long-chain fatty acyl residues. Lipid-containing outer membrane vesicles are important vehicles for the delivery of bacterial effector proteins and quorum sensing via a-hydroxyketone signaling molecules is important for virulence. Besides contributing to virulence with its own lipids, L. pneumophila also interferes with the metabolism of host cell membranes and specifically redirects phosphoinositide-controlled signaling pathways thereby facilitating its replication and spread within its host.
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Introduction
Legionella pneumophila is a Gram-negative facultative intracellular pathogen, which multiplies in protozoa in its natural environment. The virulence mechanisms evolved by L. pneumophila, also enable its attachment to as well as survival and replication inside human macrophages and infection of alveolar macrophages can cause Legionnaires’ disease, a severe form of pneumonia in man. In each of the different infection stages of host cells, virulence proteins need to be delivered to their specific place of action and this is achieved by several specialized secretion machineries (De Buck et al., 2007). Most importantly, a type IV secretion system, which translocates a large repertoire of bacterial effectors into the host cell is indispensable for L. pneumophila’s intracellular survival. The effectors modulate multiple host cell processes, redirect trafficking of the L. pneumophila phagosome and mediate its conversion into an endoplasmatic reticulum-derived organelle that permits intracellular bacterial replication (Shin and Roy, 2008). When nutrients are depleted, the bacteria enter the transmissive phase, and express virulence proteins, resulting in lysis of host cells and the initiation of a new infection round (Steinert et al., 2007). To date most of the focus has been on how Legionella proteins contribute to bacterial virulence. It is becoming clear, however, that also specific Legionella lipids are important determinants for virulence.
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Membrane-forming Lipids in Legionella pneumophila
In the bacterial model organism, Escherichia coli, only the three major membrane lipids phosphatidylethanolamine, phosphatidylglycerol, and cardiolipin occur (Rock,
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