AI Article Synopsis

  • Scientists studied bacteria called L. pneumophila, which can live in human cells and avoid getting destroyed.
  • They tested different bacterial mutants to see which ones can't stop these bacteria from mixing with cell trash-collecting parts called lysosomes.
  • They found some interesting proteins that help L. pneumophila survive and possibly why it spreads, which could help understand how it causes illness called Legionnaires' disease.

Article Abstract

L. pneumophila-containing vacuoles (LCVs) exclude endocytic and lysosomal markers in human macrophages and protozoa. We screened a L. pneumophila mini-Tn10 transposon library for mutants, which fail to inhibit the fusion of LCVs with lysosomes by loading of the lysosomal compartment with colloidal iron dextran, mechanical lysis of infected host cells, and magnetic isolation of LCVs that have fused with lysosomes. In silico analysis of the mutated genes, D. discoideum plaque assays and infection assays in protozoa and U937 macrophage-like cells identified well established as well as novel putative L. pneumophila virulence factors. Promising candidates were further analyzed for their co-localization with lysosomes in host cells using fluorescence microscopy. This approach corroborated that the O-methyltransferase, PilY1, TPR-containing protein and polyketide synthase (PKS) of L. pneumophila interfere with lysosomal degradation. Competitive infections in protozoa and macrophages revealed that the identified PKS contributes to the biological fitness of pneumophila strains and may explain their prevalence in the epidemiology of Legionnaires' disease.

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http://dx.doi.org/10.1016/j.ijmm.2014.08.010DOI Listing

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