<i>Pseudomonas aeruginosa</i> quorum sensing molecule <i>N</i>‐(3 oxododecanoyl)‐<scp>l</scp>‐homoserine lactone disrupts epithelial barrier integrity of Caco‐2 cells

Vikström, Elena; Tafazoli, Farideh; Magnusson, Karl‐Eric

doi:10.1016/j.febslet.2006.11.057

Cited by 77 publications

(72 citation statements)

References 36 publications

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“…Previous data from our group and others have shown how this AHL communication affect human host cells such as migration and phagocytosis [4,147,152,155,156,188,225,237,238]. In cell motility the aquaporins play an important role for the formation membrane protrusions [17,40,58,77,80].…”

Section: Resultsmentioning

confidence: 99%

Aquaporins in Infection and Inflammation

Holm¹

2016

Linköping University Medical Dissertations

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About the cover:The front cover displays a human, blood-derived macrophage stained for aquaporin 9.During the course of the research underlying this thesis, Angelika Holm was enrolled in Forum Scientium, a multidisciplinary doctoral programme at Linköping University Printed by LiU-Tryck, Linköping, Sweden, 2016 "Be brave, even if you're not, pretend to be. No one can tell the difference."To that young, awkward, tall girl who dared to dream of something else, something more:You did it. SUPERVISOR Elena VikströmDepartment of Clinical and Experimental Medicine Linköping University Linköping Sweden When cells of the innate immune system encounter pathogens they need to respond and prepare for migration and phagocytosis and do so through volume regulatory processes. The Gramnegative bacterium Pseudomonas aeruginosa utilizes a small molecule-based communication system, called quorum sensing (QS) to control the production of its virulence factors and biofilms. We found that P. aeruginosa with a complete QS system elicits a stronger phagocytic response in human blood-derived macrophages compared to its lasI-/rhlI-mutant lacking the production of the QS molecules N-butyryl-L-homoserine lactone (C4-HSL) and N-3-oxododecanoyl-L-homoserine lactone (3O-C12-HSL). Infection with P. aeruginosa further increases the expression of AQP9 and induces re-localisation of AQP9 to the front and trailing ends of macrophages. Moreover, the 3O-C12-HSL alone elevates the expression of AQP9, redistribute the water channel to the front and rear ends and increases the cell area and volume of macrophages. Both infection with the wild type P. aeruginosa and the treatment with 3O-C12-HSL change the nano-structural architecture of the AQP9 distribution in macrophages. ASSISTANT SUPERVISORS Karl-Eric MagnussonViruses use the intracellular machinery of the invaded cells to produce and assemble new viral bodies. Intracellular AQPs are localised in a membranes of cellular organelles to regulate their function and morphology. C3H10T1/2 fibroblasts transiently expressing green fluorescent protein (GFP)-AQP6 show a reduced expression of AQP6 after Hazara virus infection and an increased cell area. Overexpressing AQP6 in C3H10T1/2 cells reduces the infectivity of Hazara virus indicating that AQP6 expression has a protective role in virus infections.Ion and water channels in the epithelial cell lining tightly regulate the water homeostasis. In microscopic colitis (MC), patients suffer from severe watery diarrhoeas. For the first time, we have shown that the expression of AQP1, 8 and 11 and the sodium/hydrogen exchanger NHE1 are reduced in colonic biopsies from MC patients compared to healthy control individuals. Following treatment with the glucocorticoid budesonide the patients experienced a rapid recovery and we observed a restored or increased expression of the AQPs and NHE1 during treatment, suggesting a role for AQPs in the diarrhoeal mechanisms in MC.Taken together, this thesis provides new evidence on the importance of water homeostasis regulatio...

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Section: Resultsmentioning

confidence: 99%

Aquaporins in Infection and Inflammation

Holm¹

2016

Linköping University Medical Dissertations

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“…Similarly, a large number of previous studies have also reported that disruption of tight junction by oxidants, pathogens and proinflammatory cytokines in various epithelial cells caused declined TER, which was associated with downregulation of occludin and ZO-1. 12,15,21,30,[36][37][38] Our findings indicated that COM crystals caused increased permeability and defective barrier function of tight junction of renal tubular epithelial cells.…”

Section: Zo-1 Occludinmentioning

confidence: 99%

“…Our data were consistent to those reported in previous studies demonstrating that various stimuli (including oxidative stress, proinflammatory cytokines and pathogens) caused downregulation of occludin and ZO-1 in MDCK and Caco-2 cells. 17,30,[36][37][38] Immunofluorescence studies revealed not only downregulation but also redistribution and dissociation of these two proteins (Figure 3), indicating disruption of tight junction complex. These data were also in concordance with findings of a recent study illustrating that H 2 O 2 -induced disruption of tight junction caused redistribution of occludin and ZO-1 from intercellular junction into cytoplasmic compartment of Caco-2 and T84 cells.…”

Section: Zo-1 Occludinmentioning

confidence: 99%

Effects of calcium oxalate monohydrate crystals on expression and function of tight junction of renal tubular epithelial cells

Peerapen

Thongboonkerd

2011

Laboratory Investigation

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“…However, specific molecules responsible for such protective actions are yet to be identified. In contrast, quorum sensing molecules such as the N-(3-oxododecanoyl)-L-homoserine lactone produced by Pseudomonas aeruginosa have been shown to be deleterious to host cells, in that it helps promote persistent infection by disrupting cell barrier properties, and upregulating inflammatory pathways [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Role for the Bacterial Signal Indole in Promoting Epithelial Cell Barrier Function

Bansal¹

2012

JEBP

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Interkingdom (IK) signaling, in which pathogenic bacteria recognize human hormones in the gastrointestinal tract to initiate infection, has recently emerged as an important contributor to gastrointestinal tract infections. While a majority of studies have primarily focused on the effect of host molecules on pathogens, recent work from our lab has demonstrated that human intestinal epithelial cells can also recognize bacterial signaling molecules. We demonstrated that indole, secreted to ~ 500 M by commensal Escherichia coli, increased expression of tight junction proteins and genes involved in mucin production in HCT-8 intestinal epithelial cells, thus enhancing their barrier properties. These results were consistent with an observed increased in trans-epithelial resistance on exposure to indole over 24 h. Since indole is structurally similar to melatonin, and melatonin is a hormone that regulates the dark-cycle in the eye, we also investigated role of indole on human retinal pigment epithelium (RPE) cells. Our data show that indole increases trans-epithelial resistance of RPE cells, and attenuated their proliferation and migration. Our results suggest a beneficial role for indole in the treatment of eye diseases, and are discussed in detail in this article.

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Pseudomonas aeruginosa quorum sensing molecule N‐(3 oxododecanoyl)‐l‐homoserine lactone disrupts epithelial barrier integrity of Caco‐2 cells

Cited by 77 publications

References 36 publications

Aquaporins in Infection and Inflammation

Aquaporins in Infection and Inflammation

Effects of calcium oxalate monohydrate crystals on expression and function of tight junction of renal tubular epithelial cells

Role for the Bacterial Signal Indole in Promoting Epithelial Cell Barrier Function

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