Bacterial Invasion: The Paradigms of Enteroinvasive Pathogens

Cossart, Pascale; Sansonetti, Philippe J.

doi:10.1126/science.1090124

Cited by 888 publications

(876 citation statements)

References 60 publications

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“…From left to right: reconstitution of the type III secretion system; scanning electron micrograph of Shigella entering into cells. These images are adapted from [Cossart and Sansonetti, 2004;Niemann et al, 2007;Schubert et al, 2002].…”

Section: Introductionmentioning

confidence: 99%

Cytoskeleton rearrangements during Listeria infection: Clathrin and septins as new players in the game

Mostowy

Cossart

2009

Cell Motil. Cytoskeleton

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The study of an infection process can reveal how microbes exploit the host, and can illuminate unknown host cellular functions. Invasive pathogens have evolved efficient strategies to promote their internalization within normally non-phagocytic host cells. The so-called ''zippering'' bacteria present to host cell receptors molecules that mimic endogenous ligands, thereby inducing specific intracellular signaling cascades ultimately resulting in actin polymerization and uptake. Here we review how the bacterial pathogen Listeria monocytogenes enters into cells, and present a series of studies revealing that in addition to actin rearrangements this bacterium exploits the clathrin-mediated endocytosis machinery together with septins, a novel cytoskeleton element. The challenge is now to decipher how all of these components orchestrate themselves to permit entry into normally non-phagocytic cells. Cell Motil. Cytoskeleton 66: 816-823, 2009. '

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Section: Introductionmentioning

confidence: 99%

Cytoskeleton rearrangements during Listeria infection: Clathrin and septins as new players in the game

Mostowy

Cossart

2009

Cell Motil. Cytoskeleton

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“…The mechanism behind this evasion is poorly understood and is likely specific to each bacterium. F. tularensis, Listeria monocytogenes, and Salmonella enterica all alter or escape the macrophage phagolysosomes to evade destruction (26,27). Some intracellular bacteria down-regulate MHC class I or MHC class II surface expression (28 -31).…”

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confidence: 99%

Francisella tularensis-Infected Macrophages Release Prostaglandin E2 that Blocks T Cell Proliferation and Promotes a Th2-Like Response

Woolard

Wilson

Hensley

et al. 2007

The Journal of Immunology

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Francisella tularensis is a highly infectious bacterial pathogen, and is likely to have evolved strategies to evade and subvert the host immune response. In this study, we show that F. tularensis infection of macrophages alters T cell responses in vitro, by blocking T cell proliferation and promoting a Th2-like response. We demonstrate that a soluble mediator is responsible for this effect and identify it as PGE2. Supernatants from F. tularensis-infected macrophages inhibited IL-2 secretion from both MHC class I and MHC class II-restricted T cell hybridomas, as well as enhanced a Th2-like response by inducing increased production of IL-5. Furthermore, the soluble mediator blocked proliferation of naive MHC class I-restricted T cells when stimulated with cognate tetramer. Indomethacin treatment partially restored T cell proliferation and lowered IL-5 production to wild-type levels. Macrophages produced PGE2 when infected with F. tularensis, and treatment of infected macrophages with indomethacin, a cyclooxygenase-1/cyclooxygenase-2 inhibitor, blocked PGE2 production. To further demonstrate that PGE2 was responsible for skewing of T cell responses, we infected macrophages from membrane PGE synthase 1 knockout mice (mPGES1−/−) that cannot produce PGE2. Supernatants from F. tularensis-infected membrane PGE synthase 1−/− macrophages did not inhibit T cell proliferation. Furthermore, treatment of T cells with PGE2 recreated the effects seen with infected supernatant. From these data, we conclude that F. tularensis can alter host T cell responses by causing macrophages to produce PGE2. This study defines a previously unknown mechanism used by F. tularensis to modulate adaptive immunity.

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“…Alternatively, bacteria that possess a type III secretion system directly inject protein effectors into the host cytosol, avoiding initial intimate contact with the host cell. These effectors trigger massive actin polymerization and the formation of macropinocytic membrane extensions that lead to bacterial internalization ('trigger' mechanisms) (Cossart & Sansonetti, 2004;Veiga & Cossart, 2006). With regard to T. forsythia, the genome sequence (available at http://www.oralgen.lanl.gov) does not predict the presence of a conventional type III secretion system in the bacterium.…”

Section: Introductionmentioning

confidence: 99%

“…In this regard, pathogens are known to usurp host cellular machinery for entry. A majority of bacteria that invade non-phagocytic cells express surface proteins that interact with cellular receptors to initiate signalling cascades that result in membrane 'zippering' for entry (Cossart & Sansonetti, 2004;Veiga & Cossart, 2006). Alternatively, bacteria that possess a type III secretion system directly inject protein effectors into the host cytosol, avoiding initial intimate contact with the host cell.…”

Section: Introductionmentioning

confidence: 99%

Tannerella forsythia invasion in oral epithelial cells requires phosphoinositide 3-kinase activation and clathrin-mediated endocytosis

Mishima

Sharma

2011

Microbiology

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Tannerella forsythia, a Gram-negative anaerobe implicated in periodontitis, has been detected within human buccal epithelial cells and shown to invade oral epithelial cells in vitro. We have previously shown that this bacterium triggers host tyrosine kinase-dependent phosphorylation and actin-dependent cytoskeleton reorganization for invasion. On the bacterial side, the leucine-rich repeat cell-surface BspA protein is important for entry. The present study was undertaken to identify host signalling molecules during T. forsythia entry into human oral and cervical epithelial cells. Specifically, the roles of phosphatidylinositol 3-kinase (PI3K), Rho-family GTPases, cholesterol-rich membrane microdomains and the endocytic protein clathrin were investigated. For this purpose, cell lines were pretreated with chemical inhibitors or small interfering RNAs (siRNAs) that target PI3Ks, Rho GTPases, clathrin and cholesterol (a critical component of ‘lipid rafts’), and the resulting effects on T. forsythia uptake were determined. Our studies revealed that T. forsythia entry is dependent on host PI3K signalling, and that purified BspA protein causes activation of this lipid kinase. Bacterial entry also requires the cooperation of host Rac1 GTPase. Finally, our findings indicate an important role for clathrin and cholesterol-rich lipid microdomains in the internalization process

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Bacterial Invasion: The Paradigms of Enteroinvasive Pathogens

Cited by 888 publications

References 60 publications

Cytoskeleton rearrangements during Listeria infection: Clathrin and septins as new players in the game

Cytoskeleton rearrangements during Listeria infection: Clathrin and septins as new players in the game

Francisella tularensis-Infected Macrophages Release Prostaglandin E2 that Blocks T Cell Proliferation and Promotes a Th2-Like Response

Tannerella forsythia invasion in oral epithelial cells requires phosphoinositide 3-kinase activation and clathrin-mediated endocytosis

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