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Bacterial pathogenesis

Entry through a lipid zipper

Nature Reviews Microbiology volume 12, page 657 (2014)Cite this article

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It has been suggested that entry of bacterial pathogens into host cells depends on actin polymerization-driven deformation of the plasma membrane as well as additional host and bacterial factors. A new study now shows that binding of the host cell membrane component glycosphingolipid Gb3 to the bacterial surface lectin LecA is sufficient for the engulfment of the opportunistic pathogen Pseudomonas aeruginosa. LecA–Gb3 interactions induced cholesterol-dependent formation of a 'lipid zipper' at the membrane, which led to membrane invagination and bacterial invasion. Importantly, actin polymerization was not required for the formation of plasma membrane invaginations. In summary, this study shows that LecA and Gb3 are key factors that promote invasion of P. aeruginosa and are potential drug targets.

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References

  1. Eierhoff T. et al. A lipid zipper triggers bacterial invasion. Proc. Natl Acad. Sci. USA 111, 12895–12900 (2014)

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  1. Andrea Du Toit
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Du Toit, A. Entry through a lipid zipper. Nat Rev Microbiol 12, 657 (2014). https://doi.org/10.1038/nrmicro3358

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