Rickettsial interactions with human endothelial cells in vitro: adherence and entry

Walker, T S

doi:10.1128/iai.44.2.205-210.1984

Cited by 99 publications

(43 citation statements)

References 41 publications

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“…GBS invade HUVE cells significantly more than a noninvasive strain of E. coli but less than a clinical isolate of S. aureus. As shown previously for other pathogens (11,14,25,37), the entry of GBS into HUVE cells is inhibited by cytochalasin D in a dose-dependent manner. We conclude that microfilaments are necessary for endothelial uptake of GBS.…”

Section: Discussionsupporting

confidence: 82%

Group B streptococci invade endothelial cells: type III capsular polysaccharide attenuates invasion

et al. 1993

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Group B streptococci (GBS) are the most common cause of neonatal sepsis and pneumonia. The pathogenesis of GBS disease is not completely defined. GBS-induced endothelial cell injury is suggested by histological findings at autopsy and in animal studies. We hypothesized that (i) type III GBS (COH-1) invade and injure human umbilical vein endothelial (HUVE) cells and (ii) isogenic mutations in GBS capsule synthesis would influence HUVE invasion. Confluent HUVE monolayers were infected for 0.5, 2, or 6 h. Media with penicillin plus gentamicin were added and incubated for 2 h to kill extracellular bacteria. Cells were washed and lysed, and the number of live intracellular bacteria was determined by plate counting. COH-1 invaded HUVE cells in a time-dependent manner at levels 1,000-fold higher than those of the noninvasive Escherichia coli strain but significantly lower than those of Staphylococcus aureus. There was no evidence for net intracellular replication of GBS within HUVE cells. COH-1 infection of HUVE cells caused the release of lactate dehydrogenase activity. GBS invasion was inhibited by cytochalasin D in a dose-dependent manner; GBS-induced lactate dehydrogenase release was attenuated by cytochalasin D. The isogenic strains COH 1-11, devoid of capsular sialic acid, and COH 1-13, devoid of all type III capsule, invaded HUVE cells threeto fivefold more than the parent COH-1 strain. The type Ill capsular polysaccharide and particularly the capsular sialic acid attenuate GBS invasion of HUVE cells. Electron micrographs of lung tissue from a GBS-infected newborn Macaca nemestrina also showed GBS within capillary endothelial cells. We conclude that endothelial cell invasion and injury are potential mechanisms in the pathogenesis of GBS disease.

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Section: Discussionsupporting

confidence: 82%

Group B streptococci invade endothelial cells: type III capsular polysaccharide attenuates invasion

et al. 1993

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“…Invasion of host cells by Rickettsia has been reported to occur within 5 min to 2 h post infection (Walker and Winkler, 1978;Walker, 1984;Teysseire et al, 1995;Martinez and Cossart, 2004). To determine the kinetics of R. parkeri invasion, we infected immortalized human microvascular endothelial cells (HMEC-1), African green monkey kidney-derived cells (COS-7), and adherent Drosophila embryo-derived haemocyte-like cells (S2R+) with R. parkeri and determined the percentage of internalized bacteria at various times post infection by differential fluorescence staining of internal and external bacteria (Fig.…”

Section: R Parkeri Invasion Of Drosophila and Mammalian Cells Is Rapmentioning

confidence: 99%

Rickettsia parkeri invasion of diverse host cells involves an Arp2/3 complex, WAVE complex and Rho-family GTPase-dependent pathway

Reed¹,

Serio²,

Welch³

2012

Cellular Microbiology

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SUMMARY Rickettsiae are obligate intracellular pathogens that are transmitted to humans by arthropod vectors and cause diseases such as spotted fever and typhus. Although rickettsiae require the host cell actin cytoskeleton for invasion, the cytoskeletal proteins that mediate this process have not been completely described. To identify the host factors important during cell invasion by Rickettsia parkeri, a member of the spotted fever group (SFG), we performed an RNAi screen targeting 105 proteins in Drosophila melanogaster S2R+ cells. The screen identified 21 core proteins important for invasion, including the GTPases Rac1 and Rac2, the WAVE nucleation promoting factor complex and the Arp2/3 complex. In mammalian cells, including endothelial cells, the natural targets of R. parkeri, the Arp2/3 complex was also crucial for invasion, while requirements for WAVE2 as well as Rho GTPases depended on the particular cell type. We propose that R. parkeri invades S2R+ arthropod cells through a primary pathway leading to actin nucleation, whereas invasion of mammalian endothelial cells occurs via redundant pathways that converge on the host Arp2/3 complex. Our results reveal a key role for the WAVE and Arp2/3 complexes, as well as a higher degree of variation than previously appreciated in actin nucleation pathways activated during Rickettsia invasion.

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“…To date, in vivo experiments have not been described with R. prowazekii or R. typhi . Uptake of Rickettsia also requires participation of the parasitized host as it is mediated by an induced phagocytosis process [92,93]. A rickettsial phospholipase A 2 (PLA 2 ) has been proposed to mediate escape from phagosomes [27,94].…”

Section: Virulence Factorsmentioning

confidence: 99%

Some lessons fromRickettsiagenomics

Renesto¹,

Ogata²,

Audic³

et al. 2005

FEMS Microbiol Rev

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Sequencing of the Rickettsia conorii genome and its comparison with its closest sequenced pathogenic relative, i.e., Rickettsia prowazekii, provided powerful insights into the evolution of these microbial pathogens. However, advances in our knowledge of rickettsial diseases are still hindered by the difficulty of working with strict intracellular bacteria and their hosts. Information gained from comparing the genomes of closely related organisms will shed new light on proteins susceptible to be targeted in specific diagnostic assays, by new antimicrobial drugs, and that could be employed in the generation of future rickettsial vaccines. In this review we present a detailed comparison of the metabolic pathways of these bacteria as well as the polymorphisms of their membrane proteins, transporters and putative virulence factors. Environmental adaptation of Rickettsia is also discussed.

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Rickettsial interactions with human endothelial cells in vitro: adherence and entry

Cited by 99 publications

References 41 publications

Group B streptococci invade endothelial cells: type III capsular polysaccharide attenuates invasion

Group B streptococci invade endothelial cells: type III capsular polysaccharide attenuates invasion

Rickettsia parkeri invasion of diverse host cells involves an Arp2/3 complex, WAVE complex and Rho-family GTPase-dependent pathway

Some lessons fromRickettsiagenomics

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