Pseudomonas aeruginosa induces apoptosis in human endothelial cells

Valente, Liz J.; Assis, Monique Ribeiro de; Alvim, Iris Maria Peixoto; Pereira, Geraldo M. B.; Plotkowski, Maria-Cristina

doi:10.1006/mpat.2000.0400

Cited by 42 publications

(27 citation statements)

References 38 publications

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“…Infection with P. aeruginosa 762 at 37°C yielded rapid induction of apoptosis accompanied by CD95-upregulation, mitochondrial alterations and exposure of phosphatidylserine on the surface of the infected cells. These results confirm earlier reports on the involvement of mitochondrial alterations and the production of reactive oxygen species in the induction of apoptosis after infection of epithelial or endothelial cells with P. aeruginosa [8,12]. However, after infection at 22°C, P. aeruginosa failed to induce significant apoptosis or mitochondrial alterations.…”

Section: Discussionsupporting

confidence: 81%

<i>Pseudomonas Aeruginosa</i> Triggered Apoptosis of Human Epithelial Cells Depends on the Temperature During Infection

Fillon¹,

Läng²,

Jendrossek³

2002

Cell Physiol Biochem

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The induction of apoptosis is a hallmark in many bacterial infections. Here, we show that the environmental temperature during infection influences P. aeruginosainduced apoptosis in human conjunctiva epithelial Chang cells. Infection with the clinical isolate P. aeruginosa762 at 37°C resulted in a rapid induction of apoptosis within 30 min. Apoptosis was mediated by upregulation of CD95-receptor expression on the surface of the infected cells and depolarisation of the mitochondrial membrane potential (ΔΨm) as determined by FACS-analysis of immunostained cells or of cells loaded with the potential sensitive dye JC1 respectively. In contrast, P. aeruginosafailed to induce significant apoptosis and mitochondrial alterations at 22°C. The loss of the apoptotic response at 22°C correleated with the failure of the epithelial cells to upregulate CD95, while bacterial growth or secretion of bacterial exotoxins into the culture supernatant appeared to be not affected. From our data we conclude that P. aeruginosa762 induced apoptosis is dependent on the temperature during infection and that cellular pathways leading to CD95-upregulation are inhibited at low temperature.

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Section: Discussionsupporting

confidence: 81%

<i>Pseudomonas Aeruginosa</i> Triggered Apoptosis of Human Epithelial Cells Depends on the Temperature During Infection

Fillon¹,

Läng²,

Jendrossek³

2002

Cell Physiol Biochem

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“…A prolonged exposure to bacteria and inflammation may predispose host tissues to greater damage, which in turn may modulate vessel formation and further amplify the inflammation. Previous studies have shown that bacterial challenge with Pseudomonas aeruginosa (13), Porphyromonas gingivalis (14), and Enterococcus faecalis (15) modulates endothelial cell function. Data also suggest that endothelial cells respond to P. gingivalis by increasing the levels of leukocyte adhesion molecules, elevating levels of inflammatory cytokines and chemokines, and inducing prothrombotic properties (16,17).…”

mentioning

confidence: 98%

Endothelial Cell Response to Fusobacterium nucleatum

Mendes

Nguyen²,

Stephens³

et al. 2016

Infect Immun

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c Vascular response is an essential aspect of an effective immune response to periodontal disease pathogens, as new blood vessel formation contributes to wound healing and inflammation. Gaining a greater understanding of the factors that affect vascular response may then contribute to future breakthroughs in dental medicine. In this study, we have characterized the endothelial cell response to the common bacterium Fusobacterium nucleatum, an important bridging species that facilitates the activity of late colonizers of the dental biofilm. Endothelial cells were infected with Fusobacterium nucleatum (strain 25586) for periods of 4, 12, 24, or 48 h. Cell proliferation and tube formation were analyzed, and expression of adhesion molecules (CD31 and CD34) and vascular endothelial growth factor (VEGF) receptors 1 and 2 was measured by fluorescenceactivated cell sorter (FACS) analysis. Data indicate that F. nucleatum impaired endothelial cell proliferation and tube formation. The findings suggest that the modified endothelial cell response acts as a mechanism promoting the pathogenic progression of periodontal diseases and may potentially suggest the involvement of periodontopathogens in systemic diseases associated with periodontal inflammation.

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“…has also been found to induce apoptosis in epithelial cells (7) and endothelial cells (27). In this report, we investigated whether the Pa IID1117 and Pa IID1130 strains have a cytotoxic effect on macrophage cell line J774 and induce apoptosis in the cells.…”

mentioning

confidence: 98%

Induction of Apoptosis in Macrophage Cell Line, J774, by the Cell‐Free Supernatant from Pseudomonas aeruginosa

Zhang

Takayama

Matsuba

et al. 2003

Microbiology and Immunology

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Pseudomonas aeruginosa is able to secrete many virulence factors that are cytotoxic towards eukaryotic cells. To investigate the effect of the bacterium on macrophages, we obtained cell‐free supernatants from P. aeruginosa (Pa) IID1117 (elastase‐positive and protease‐positive) and Pa IID1130 (elastase‐positive and protease‐negative). After 6 hr of incubation with the cell‐free supernatant from the Pa IID1117 strain, the viability of J774 macrophages was shown to be significantly reduced (47.5±11%), but not Pa IID1130 (96.4±1.6%) at a concentration of 10% (v/v) compared to control J774 macrophages without any supernatant (97.2±1.7%) by the detection of trypan blue dye exclusion. The death of cells was further demonstrated to be due to apoptosis characterized by chromatin condensation and apoptotic bodies by Hoechst 33258 staining, DNA fragmentation by agarose gel electrophoresis and terminal deoxynucleotidyl transferase‐mediated d‐UTP nick end labeling (TUNEL). An activated subunit was found to be released from procaspase‐3 in cell lysate. But in the presence of protease inhibitor, the apoptosis was completely blocked. The findings indicate that the Pa IID1117 strain is capable of inducing apoptosis in J774 macrophages. The apoptosis induced by the cell‐free supernatant from Pa IID1117 strain is suggested to be dependent on protease, but not elastase.

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Pseudomonas aeruginosa induces apoptosis in human endothelial cells

Cited by 42 publications

References 38 publications

<i>Pseudomonas Aeruginosa</i> Triggered Apoptosis of Human Epithelial Cells Depends on the Temperature During Infection

<i>Pseudomonas Aeruginosa</i> Triggered Apoptosis of Human Epithelial Cells Depends on the Temperature During Infection

Endothelial Cell Response to Fusobacterium nucleatum

Induction of Apoptosis in Macrophage Cell Line, J774, by the Cell‐Free Supernatant from Pseudomonas aeruginosa

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