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Science 18 June 2004:
Vol. 304. no. 5678, pp. 1805 - 1807
DOI: 10.1126/science.1098188
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Reports

Salmonella Modulates Vesicular Traffic by Altering Phosphoinositide Metabolism

Lorraine D. Hernandez,1* Karsten Hueffer,1 Markus R. Wenk,2{dagger} Jorge E. Galán1{ddagger}

Salmonella enterica, the cause of food poisoning and typhoid fever, induces actin cytoskeleton rearrangements and membrane ruffling to gain access into nonphagocytic cells, where it can replicate and avoid innate immune defenses. Here, we found that SopB, a phosphoinositide phosphatase that is delivered into host cells by a type III secretion system, was essential for the establishment of Salmonella's intracellular replicative niche. SopB mediated the formation of spacious phagosomes following bacterial entry and was responsible for maintaining high levels of phosphatidylinositol-three-phosphate [PtdIns(3)P] in the membrane of the bacteria-containing vacuoles. Absence of SopB caused a significant defect in the maturation of the Salmonella-containing vacuole and impaired bacterial intracellular growth.

1 Section of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06536, USA.
2 Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06510, USA.


* Present address: Department of Human and Animal Infectious Disease, Merck Research Laboratories, Rahway, NJ 07065, USA.

{dagger} Present address: Department of Biochemistry, National University of Singapore, 8 Medical Drive, Singapore 117597.

{ddagger} To whom correspondence should be addressed. E-mail: jorge.galan{at}yale.edu

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