Cholera toxin and extracellular Ca2+ induce adherence of non-piliated Neisseria: evidence for an important role of G-proteins and Rho in the bacteria-cell interaction

Källström, Helena; Hansson‐Palo, Paola; Jonsson, Ann‐Beth

doi:10.1046/j.1462-5822.2000.00063.x

Cited by 9 publications

(4 citation statements)

References 59 publications

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“…It is generally accepted that the interaction between the pathogenic microorganism and the host cell plays a critical role in many infectious diseases [22][23][24]. Attachment to host cell is usually the Wrst step for disease development caused by bacteria such as Vibrio cholera [25], Salmonella and Shigella [26,27].…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of leptospirosis: interaction of Leptospira interrogans with in vitro cultured mammalian cells

Liu

Zheng

et al. 2007

Med Microbiol Immunol

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Interactions of virulent Leptospira interrogans with murine monocyte-macrophage-like J774A.1 cells and Vero (African green monkey kidney fibroblasts) cells from attachment to internalization were investigated by a series of morphological analysis. Fontana silver staining revealed that only the pathogenic leptospires were able to attach to host cells and the attachment pattern varied depending on cell types that they interacted with. Transmission electron microscopy (TEM) analysis confirmed the formation of the leptospires-containing phagosomes and their colocalization with lysosomes in macrophages were verified by confocal microscopic analysis. Results of F-actin rearrangements examination indicated that virulent leptospires invaded host cells via a microfilament-independent pathway.

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Section: Discussionmentioning

confidence: 99%

Pathogenesis of leptospirosis: interaction of Leptospira interrogans with in vitro cultured mammalian cells

Liu

Zheng

et al. 2007

Med Microbiol Immunol

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“…The initial attachment of the bacteria to the apical surface of epithelial tissues is mediated by type IV pili (Källström et al, 1997;Merz et al, 1999;Merz et al, 1996;Swanson, 1973). The adherence mediates host cell-signaling events and elicits a multitude of cellular responses, including cortical plaque formation (Merz et al, 1999), the release of intracellular calcium (Källström et al, 2000;Källström et al, 1998), and the induction of anti-apoptotic factors (Binnicker et al, 2003;Follows et al, 2009). During N. gonorrhoeae infection, several signaling pathways are induced by virulence factors such as porins, lipooligosaccharides, iron receptors, outer membrane vesicles, and pilus biogenesis-associated proteins (for reviews, see Popp et al, 2001;Koomey, 2001).…”

Section: Introductionmentioning

confidence: 99%

Neisseria gonorrhoeae infection causes DNA damage and affects the expression of p21, p27 and p53 in non-tumor epithelial cells

Vielfort

Söderholm

Weyler

et al. 2013

Journal of Cell Science

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SummaryThe constant shedding and renewal of epithelial cells maintain the protection of epithelial barriers. Interference with the processes of host cell-cycle regulation and barrier integrity permits the bacterial pathogen Neisseria gonorrhoeae to effectively colonize and invade epithelial cells. Here, we show that a gonococcal infection causes DNA damage in human non-tumor vaginal VK2/E6E7 cells with an increase of 700 DNA strand breaks per cell per hour as detected by an alkaline DNA unwinding assay. Infected cells exhibited elevated levels of DNA double-strand breaks, as indicated by a more than 50% increase in cells expressing DNA damage-response protein 53BP1-positive foci that co-localized with phosphorylated histone H2AX (cH2AX). Furthermore, infected cells abolished their expression of the tumor protein p53 and induced an increase in the expression of cyclin-dependent kinase inhibitors p21 and p27 to 2.6-fold and 4.2-fold of controls, respectively. As shown by live-cell microscopy, flow cytometry assays, and BrdU incorporation assays, gonococcal infection slowed the host cell-cycle progression mainly by impairing progression through the G2 phase. Our findings show new cellular players that are involved in the control of the human cell cycle during gonococcal infection and the potential of bacteria to cause cellular abnormalities.

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“…Initial attachment of the bacteria to the apical side of epithelial tissues is mediated by type IV pili [1], [2], [3], [4]. The adherence mediates host cell signaling events and elicits a multitude of cellular responses, including cortical plaque formation [3], release of intracellular calcium [5], [6] and anti apoptotic factors [7], [8].…”

Section: Introductionmentioning

confidence: 99%

Neisseria gonorrhoeae Infection Induces Altered Amphiregulin Processing and Release

2011

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Adhesion of the human pathogen Neisseria gonorrhoeae has established effects on the host cell and evokes a variety of cellular events including growth factor activation. In the present study we report that infection with N. gonorrhoeae causes altered amphiregulin processing and release in human epithelial cells. Amphiregulin is a well-studied growth factor with functions in various cell processes and is upregulated in different forms cancer and proliferative diseases. The protein is prototypically cleaved on the cell surface in response to external stimuli. We demonstrate that upon infection, a massive upregulation of amphiregulin mRNA is seen. The protein changes its subcellular distribution and is also alternatively cleaved at the plasma membrane, which results in augmented release of an infection-specific 36 kDa amphiregulin product from the surface of human cervical epithelial cells. Further, using antibodies directed against different domains of the protein we could determine the impact of infection on pro-peptide processing. In summary, we present data showing that the infection of N. gonorrhoeae causes an alternative amphiregulin processing, subcellular distribution and release in human epithelial cervical cells that likely contribute to the predisposition cellular abnormalities and anti-apoptotic features of N. gonorrhoeae infections.

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Cholera toxin and extracellular Ca2+ induce adherence of non-piliated Neisseria: evidence for an important role of G-proteins and Rho in the bacteria-cell interaction

Abstract: SummaryIn this study, we characterize the interaction between non-piliated (P 2 ) Neisseria gonorrhoeae and human and reveal a novel function of cholera toxin, namely induction of bacterial adherence.

Cited by 9 publications

References 59 publications

Pathogenesis of leptospirosis: interaction of Leptospira interrogans with in vitro cultured mammalian cells

Pathogenesis of leptospirosis: interaction of Leptospira interrogans with in vitro cultured mammalian cells

Neisseria gonorrhoeae infection causes DNA damage and affects the expression of p21, p27 and p53 in non-tumor epithelial cells

Neisseria gonorrhoeae Infection Induces Altered Amphiregulin Processing and Release

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