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Review
. 1998 Sep;64(9):3127-33.
doi: 10.1128/AEM.64.9.3127-3133.1998.

Invasion of protozoa by Legionella pneumophila and its role in bacterial ecology and pathogenesis

Y Abu Kwaik  1 , L Y Gao, B J Stone, C Venkataraman, O S Harb
Affiliations
Review

Invasion of protozoa by Legionella pneumophila and its role in bacterial ecology and pathogenesis

Y Abu Kwaik et al. Appl Environ Microbiol. 1998 Sep.
No abstract available

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Figures

FIG. 1
FIG. 1
Model illustrating the signal transduction mechanisms used by L. pneumophila during invasion of its protozoan host H. vermiformis. The 170-kDa Gal/GalNAc lectin is basally tyrosine phosphorylated (YP) and is associated with several phosphorylated proteins. Several cytoskeletal proteins such as paxillin, vinculin, and focal adhesion kinase (FAK) are also tyrosine phosphorylated in resting H. vermiformis and can potentially interact with the Gal/GalNAc lectin. Attachment to and invasion of the host by L. pneumophila is mediated by noncoated-receptor-mediated endocytosis and involves an increase in bacterium-induced tyrosine phosphatase activity in H. vermiformis. This results in tyrosine dephosphorylation of several host cell proteins, including the 170-kDa Gal/GalNAc lectin and cytoskeletal proteins such as paxillin, vinculin, and focal adhesion kinase. This process is associated with disruption of the interaction between the Gal/GalNAc lectin and its associated proteins. Less than 10% of bacterial uptake is mediated by coiling phagocytosis, and we think it is unlikely that the lectin is involved in this process, since it also occurs in mammalian monocytes. The exact signaling mechanisms involved in uptake of L. pneumophila by coiling phagocytosis are not known. Bacterial entry is associated with induction of host cell gene expression, which is necessary for the invasion of H. vermiformis by L. pneumophila.
FIG. 2
FIG. 2
Transmission electron micrographs of H. vermiformis (A and B) and WI-26 type I human alveolar epithelial cells (C and D) infected with L. pneumophila AA100 at 4 h (A and C) and 12 h (B and D) postinfection. The open arrows in panels A and C indicate RER-surrounded phagosomes, while the b’s indicate bacteria. Note that the whole cell (B and D) becomes heavily infected with numerous bacteria (a few hundred to a thousand) by 18 h postinfection. Magnifications, ×20,400 (A), ×3,400 (B), ×27,200 (C), ×1,700 (D).
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References

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