Neutrophil transendothelial migration in vitro to<i>Streptococcus pneumoniae</i>is pneumolysin dependent

Moreland, Jessica G.; Bailey, Gail

doi:10.1152/ajplung.00333.2005

Cited by 33 publications

(43 citation statements)

References 34 publications

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“…1) Ft LVS interacted with and invaded PMVEC when presented at the abluminal surface of the endothelium, as would occur after an organism had traversed the alveolar epithelium en route to the bloodstream. To our knowledge, this is the first demonstration that Francisella can enter microvascular endothelial cells, behavior similar to that of another nonmotile organism, S. pneumoniae (21). Ft LVS alone did not elicit secretion of IL-8 or MCP-1 from PMVEC.…”

Section: Discussionmentioning

confidence: 57%

Francisella tularensisdirectly interacts with the endothelium and recruits neutrophils with a blunted inflammatory phenotype

Moreland¹,

Hook

Bailey

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Francisella tularensis, the causative agent of tularemia, is a highly virulent organism, especially when exposure occurs by inhalation. Recent data suggest that Francisella interacts directly with alveolar epithelial cells. Although F. tularensis causes septicemia and can live extracellularly in a murine infection model, there is little information about the role of the vascular endothelium in the host response. We hypothesized that F. tularensis would interact with pulmonary endothelial cells as a prerequisite to the clinically observed recruitment of neutrophils to the lung. Using an in vitro Transwell model system, we studied interactions between F. tularensis live vaccine strain (Ft LVS) and a pulmonary microvascular endothelial cell (PMVEC) monolayer. Organisms invaded the endothelium and were visualized within individual endothelial cells by confocal microscopy. Although these bacteria-endothelial cell interactions did not elicit production of the proinflammatory chemokines, polymorphonuclear leukocytes (PMN) were stimulated to transmigrate across the endothelium in response to Ft LVS. Moreover, transendothelial migration altered the phenotype of recruited PMN; i.e., the capacity of these PMN to activate NADPH oxidase and release elastase in response to subsequent stimulation was reduced compared with PMN that traversed PMVEC in response to Streptococcus pneumoniae. The blunting of PMN responsiveness required PMN transendothelial migration but did not require PMN uptake of Ft LVS, was not dependent on the presence of serum-derived factors, and was not reproduced by Ft LVS-conditioned medium. We speculate that the capacity of Ft LVS-stimulated PMVEC to support transendothelial migration of PMN without triggering release of IL-8 and monocyte chemotactic protein-1 and to suppress the responsiveness of transmigrated PMN to subsequent stimulation could contribute to the dramatic virulence during inhalational challenge with Francisella.

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Section: Discussionmentioning

confidence: 57%

Francisella tularensisdirectly interacts with the endothelium and recruits neutrophils with a blunted inflammatory phenotype

Moreland¹,

Hook

Bailey

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…To understand the process of transendothelial migration of prostate cancer cells, we adapted an assay commonly used to study leukocyte diapedesis (Moreland and Bailey, 2006). We plated HMVEC-L cells on a porous membrane and allowed these cells to reach confluence and establish cellcell junctions.…”

Section: Selection Of Cells Exhibiting Enhanced Temmentioning

confidence: 99%

ZEB1 Enhances Transendothelial Migration and Represses the Epithelial Phenotype of Prostate Cancer Cells

Drake

Strohbehn

Bair

et al. 2009

MBoC

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216

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Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer cells in vitro. We isolated a subpopulation of cells, TEM4-18, that crossed an endothelial barrier more efficiently, but surprisingly, were less invasive than parental PC-3 cells in other contexts in vitro. Importantly, TEM4-18 cells were more aggressive than PC-3 cells in a murine metastatic colonization model. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. Instead, TEM4-18 cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition (EMT), including frank loss of E-cadherin expression and up-regulation of the E-cadherin repressor ZEB1. Silencing ZEB1 in TEM4-18 cells resulted in increased E-cadherin and reduced transendothelial migration. TEM4-18 cells also express N-cadherin, which was found to be necessary, but not sufficient for increased transendothelial migration. Our results extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadherin in this process in prostate cancer cells. INTRODUCTIONMetastatic prostate cancer is a lethal disease and the second most frequent cause of cancer-related mortality in men in the United States (Jemal et al., 2008). Unfortunately, for such a prevalent disease, much remains unknown about the cellular and molecular mechanisms underlying prostate cancer metastasis. Extravasation, a step within the metastatic cascade, is the process whereby cancer cells exit the circulation via migration through an endothelial monolayer into the parenchyma of a secondary organ site (Wood, 1958). For extravasation to occur, cancer cells, perhaps associated with a thrombus, must first contact the microvascular endothelium, becoming entrapped in small-diameter vessels or adhering specifically to the luminal surface of the endothelium (Warren and Vales, 1972;Kramer and Nicolson, 1979). Some evidence suggests that extravasation is an efficient process, whereas other studies indicate that in some cases it might not occur at all because cancer cells proliferate intraluminally before rupturing microvessels (Crissman et al., 1985;Lapis et al., 1988;Luzzi et al., 1998). Adding to this complexity is that the mechanism of extravasation may depend on the tumor type and vascular bed involved. Thus, as with many other aspects of metastasis, questions remain about the basic mechanisms and the overall role of extravasation in the metastatic cascade.The passage of cancer cells across the endothelium, or transendothelial migration, is thought to be conceptually similar to leukocyte diapedesis (for a recent review see Miles et al., 2008). The extent to which this is true remains controversial, but several classes ...

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“…PMNs transendothelial migration were performed as described previously [12]. BrieXy, 2 £ 10 5 HBMECs were seeded on the upper chamber of Transwell insert with 5 m pore size (Corning) in 24-well plates.…”

Section: Histological Analysismentioning

confidence: 99%

Tentative identification of glycerol dehydrogenase as Escherichia coli K1 virulence factor cglD and its involvement in the pathogenesis of experimental neonatal meningitis

Zhang

Zhao

et al. 2009

Med Microbiol Immunol

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Escherichia coli (E. coli) is the most common gram-negative organism causing meningitis during the neonatal period. The mechanism involved in the pathogenesis of E. coli meningitis remains unclear. We previously identified a pathogenicity island GimA (genetic island of meningitic E. coli containing ibeA) from the genomic DNA library of E. coli K1, which may contribute to the E. coli invasion of the blood-brain barrier (BBB). CglD is one of the genes in GimA, and its function remains unknown. In order to characterize the role of cglD in the E. coli meningitis, an isogenic in-frame cglD deletion mutant of E. coli K1 was generated. The results showed that the median lethal dose of the cglD deletion mutant strain was significant higher than that of parent E. coli K1 strain, and the cglD deletion in E. coli K1 prolonged survival of the neonatal rats in experimental meningitis. However, deletion of cglD has no effect on the penetration of E. coli K1 through BBB in vitro and in vivo. Furthermore, our results showed that deletion of cglD in E. coli K1 attenuated cerebrospinal fluid changes, meningeal thickening, and neutrophil infiltration in the cerebral cortex in the neonatal rats with experimental meningitis. Additional results showed that the role of CglD in neonatal meningitis may be associated with its activity of glycerol dehydrogenase. Taken together, our study suggested that CglD is a virulence factor of E. coli K1 contributed to the development of neonatal meningitis.

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Neutrophil transendothelial migration in vitro toStreptococcus pneumoniaeis pneumolysin dependent

Cited by 33 publications

References 34 publications

Francisella tularensisdirectly interacts with the endothelium and recruits neutrophils with a blunted inflammatory phenotype

Francisella tularensisdirectly interacts with the endothelium and recruits neutrophils with a blunted inflammatory phenotype

ZEB1 Enhances Transendothelial Migration and Represses the Epithelial Phenotype of Prostate Cancer Cells

Tentative identification of glycerol dehydrogenase as Escherichia coli K1 virulence factor cglD and its involvement in the pathogenesis of experimental neonatal meningitis

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