| 1. |
- Agace, W. W., et al.
(författare)
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Escherichia coli induces transuroepithelial neutrophil migration by an intercellular adhesion molecule-1-dependent mechanism
- 1995
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Ingår i: Infection and Immunity. - 0019-9567. ; 63:10, s. 4054-4062
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Tidskriftsartikel (refereegranskat)abstract
- During bacterial infections at mucosal sites, neutrophils migrate to the mucosa and cross the epithelial barrier. We have examined neutrophil migration across Escherichia coli-stimulated uroepithelial cell layers in an attempt to more fully understand this process. Stimulation of uroepithelial cells with E. coli or interleukin-1α (IL-1α) induced transepithelial neutrophil migration in a time- and stimulant dose-dependent manner. Uroepithelial cell lines and nontransformed uroepithelial cells expressed intercellular adhesion molecule-1 (ICAM-1) but not ICAM-2, E-selectin, or P- selectin. Epithelial ICAM-1 expression was enhanced after stimulation with E. coli or IL-1α. Anti-ICAM-1 antibody reduced transepithelial neutrophil migration by 61 to 85%, indicating that neutrophils bound ICAM-1 on the epithelial surface. Antibodies to CD18 and CD11b reduced migration by 70 to 79%, suggesting that CD11b/CD18 (Mac-1) was acting as the neutrophil receptor for ICAM-1 in this process. Anti-CD11a antibodies had no effect on neutrophil migration. In conclusion, E. coli induced ICAM-1- and Mac-1-dependent transepithelial neutrophil migration. Previous studies have shown that urinary tract epithelial cells secrete IL-8 when exposed to E. coli or IL- 1α. These observations suggest that epithelial cells play an active role in neutrophil migration during urinary tract infections.
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| 2. |
- Agace, W. W.
(författare)
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The role of the epithelial cell in Escherichia coil induced neutrophil migration into the urinary tract
- 1996
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 9:8, s. 1713-1728
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Tidskriftsartikel (refereegranskat)abstract
- Neutrophil influx to mucosal surfaces represents one of the earliest inflammatory responses to mucosal infection. We have been studying external interactions with urinary tract epithelial cells in an attempt to understand the molecular mechanisms behind this process. Uropathogenic Escherichia coli induced urinary tract epithelial cells to secrete the neutrophil chemoattractant interleukin-8 (IL-8). IL-8 secretion was higher in response to isogenic strains expressing type 1 or P fimbriae that adhered to the epithelial surface. Deliberate colonization of the human urinary tract with E. coli induced the local production of IL-8 and levels correlated with urinary neutrophil numbers suggesting a role for IL-8 in neutrophil migration. E. coli induced neutrophil migration across urinary tract epithelial layers in vitro, and this process was blocked with anti-IL-8 antibody. IL-8's activity was localized to the epithelial surface. Furthermore, these cells were shown to constitutively express IL-8 receptor A and B messenger ribonucleic acid (mRNA), suggesting a possible role for IL-8 on epithelial cell function. E. coli enhanced the expression of intercellular adhesion molecule-1 (ICAM-1) on urinary tract epithelial cells, and neutrophil migration across urinary tract epithelial layers in vitro was dependent on epithelial ICAM-1 and neutrophil Mac-1 (CD11b/CD18) expression. These results suggest that bacterial/epithelial cell interactions play a key role in the induction of neutrophil migration during mucosal infection, and show the necessity for host-derived chemotactic factors and cell adhesion events in E. coli induced transuroepithelial migration in vitro.
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| 3. |
- Connell, H., et al.
(författare)
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Bacterial attachment to uro-epithelial cells : mechanisms and consequences.
- 1997
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Ingår i: Advances in dental research. - : SAGE Publications. - 0895-9374 .- 1544-0737. ; 11:1, s. 50-58
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Forskningsöversikt (refereegranskat)abstract
- Microbial attachment to mucosal surfaces is a first step in mucosal infection. Specific interactions between microbial surface ligands and host receptors influence the distribution of microbes in their sites of infection. Adhesion has often been regarded as a sufficient end point, explaining tissue tropism and bacterial persistence at mucosal sites. Adherence, however, is also a virulence factor through which microbes gain access to host tissues, upset the integrity of the mucosal barrier, and cause disease. The induction of mucosal inflammation is one aspect of this process. Bacterial attachment to mucosal surfaces activates the production of pro-inflammatory cytokines that cause both local and systemic inflammation. Epithelial cells are one source of these cytokines. The binding of fimbrial lectins to epithelial cell receptors triggers transmembrane signaling events that upregulate cytokine-specific mRNA and increase cytokine secretion. P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response. Spread of cytokines and other pro-inflammatory mediators from the local site contributes to the symptoms and signs of infection.
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| 4. |
- Connell, H., et al.
(författare)
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Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract
- 1996
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 93:18, s. 9827-9832
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Tidskriftsartikel (refereegranskat)abstract
- Type 1 fimbriae are adhesion organelles expressed by many Gram-negative bacteria. They facilitate adherence to mucosal surfaces and inflammatory cells in vitro, but their contribution to virulence has not been defined. This study presents evidence that type 1 fimbriae increase the virulence of Escherichia coli for the urinary tract by promoting bacterial persistence and enhancing the inflammatory response to infection. In a clinical study, we observed that disease severity was greater in children infected with E. coli O1:K1:H7 isolates expressing type 1 fimbriae than in those infected with type 1 negative isolates of the same serotype. The E. coli O1:K1:H7 isolates had the same electrophoretic type, were hemolysin-negative, expressed P fimbriae, and carried the fim DNA sequences. When tested in a mouse urinary tract infection model, the type 1-positive E. coli O1:K1:H7 isolates survived in higher numbers, and induced a greater neutrophil influx into the urine, than O1:K1:H7 type 1-negative isolates. To confirm a role of type 1 fimbriae, a fimH null mutant (CNI016) was constructed from an O1:K1:H7 type 1-positive parent. E. coli CNI016 had reduced survival and inflammatogenicity in the mouse urinary tract infection model. E. coli CNI016 reconstituted with type 1 fimbriae (E. coli CN1018) had restored virulence similar to that of the wild- type parent strain. These results show that type 1 fimbriae in the genetic background of a uropathogenic strain contribute to the pathogenesis of E. coli in the urinary tract.
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| 5. |
- Godaly, Gabriela, et al.
(författare)
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Role of epithelial interleukin-8 (IL-8) and neutrophil IL-8 receptor A in Escherichia coli-induced transuroepithelial neutrophil migration
- 1997
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Ingår i: Infection and Immunity. - 1098-5522. ; 65:8, s. 3451-3456
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Tidskriftsartikel (refereegranskat)abstract
- Escherichia coli stimulates neutrophil migration across human uroepithelial cell layers. This study investigated the role of the neutrophil chemokine interleukin-8 (IL-8) in this process. E. coli and IL-1alpha stimulated urinary tract epithelial layers to secrete IL-8 and induced transepithelial neutrophil migration. Anti-IL-8 antibody reduced neutrophil migration across epithelial cell layers, indicating a central role for this chemokine in the migration process. Furthermore, addition of recombinant IL-8 to unstimulated cell layers was sufficient to induce migration. The IL-8 dependence of neutrophil migration was maintained after removal of soluble IL-8 by washing of the cell layers. Flow cytometry analysis with fluorescein isothiocyanate-labelled IL-8 confirmed IL-8's ability to bind to the epithelial cell surface. Indirect immunofluorescence with confocal laser scanning microscopy showed that IL-8 associated with the epithelial cell layers. Prior incubation of neutrophils with antibodies to IL-8 receptor A (IL-8RA) reduced neutrophil migration. Anti-IL-8 RB antibody had no effect on neutrophil migration. These results demonstrate that IL-8 plays a key role in E. coli- or IL-1alpha-induced transuroepithelial migration and suggest that epithelial cell-produced IL-8 interacts with IL-8RA on the neutrophil surface.
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| 6. |
- Hedges, S., et al.
(författare)
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Cytokines induce an epithelial cell cytokine response
- 1995
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Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598. ; 371:A, s. 189-193
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Tidskriftsartikel (refereegranskat)abstract
- Intravesical inoculation of gram negative bacteria or isolated bacterial products into mice induces an IL-6 response which can be measured within miutes of the infection.1,2 In such infections, IL-6 is initially detected in the urine and subsequently in the serum. Similar IL-6 responses were found in human patients deliberately colonized in the urinary tract with E. coli Hu7343. IL-6 was secreted intermittantly into the urine in response to continuous bacterial infection in humans, but was not detected in serum. The rapid secretion of IL-6 into urine after bacterial stimulation, and the separation of local from systemic secretion in both humans and mice suggested that IL-6 was produced at the site of infection. Since epithelial cells dominate the naive urinary tract mucosal surface, we suggested that epithelial cells are one source of mucosally produced cytokines.4 Epithelial cell lines of urinary tract origin secrete IL-6 and IL-8, and can produce other cytokines after bacterial stimulation.5–7 In this paper we demonstrate that epithelial cell lines of urinary tract origin can respond to exogenous cytokines. This response includes the up-regulation of a variety of cytokine mRNA species as well as secretion of IL-6 and IL-8. Furthermore, this response is specific to the stimulus used, with different cytokine mRNA species induced by different cytokine stimuli.
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| 7. |
- Hedges, Spencer R., et al.
(författare)
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Epithelial cytokine responses and mucosal cytokine networks
- 1995
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Ingår i: Trends in Microbiology. - 0966-842X. ; 3:7, s. 266-270
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Forskningsöversikt (refereegranskat)abstract
- Localized at the border between the external environment and the internal tissue, epithelial cells are exposed to stimulants from two directions. Microorganisms in the lumen can activate the transcription of cytokine mRNA and cytokine secretion, and cytokines in the mucosal environment can modify endogenous and microbially induced epithelial cytokine responses. Epithelial cells thus actively participate in mucosal immunity and inflammation.
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