Lipids and Legionella Virulence
The intracellular lung pathogen Legionella pneumophila has evolved 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 components in its membranes which are unusual for 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 α-hydroxy ketone 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 the host.
Research in my lab was supported by grants from Consejo Nacional de Ciencia y Tecnología-México (CONACyT-Mexico) (178359 and 253549 in Investigación Científica Básica as well as 118 in Investigación en Fronteras de la Ciencia). I thank Lourdes Martínez-Aguilar for skillful technical assistance.
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