An endocytic process in HEp-2 cells induced by enteropathogenic Escherichia coli

Andrade, João Ramos Costa; Daveiga, V. F.; rosa, M.R De santa; Suassuna, I

doi:10.1099/00222615-28-1-49

Cited by 53 publications

(30 citation statements)

References 13 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This structure is composed of cytoskeletal elements such as actin filaments, a-actinin, ezrin and talin (Knutton et al, 1989;Finlay et al, 1992). EPEC is also capable of inducing its own internalization by normally non-phagocytic epithelial cells via a process termed 'invasion' (Andrade et al, 1989;Donnenberg et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Signal transduction between enteropathogenic Escherichia coli (EPEC) and epithelial cells: EPEC induces tyrosine phosphorylation of host cell proteins to initiate cytoskeletal rearrangement and bacterial uptake

Rosenshine¹,

Donnenberg²,

Kaper³

et al. 1992

Trends in Cell Biology

152

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Signal transduction between enteropathogenic Escherichia coli (EPEC) and epithelial cells: EPEC induces tyrosine phosphorylation of host cell proteins to initiate cytoskeletal rearrangement and bacterial uptake

Rosenshine¹,

Donnenberg²,

Kaper³

et al. 1992

Trends in Cell Biology

152

View full text Add to dashboard Cite

“…(iii) These signaling events culminate in the formation of attachingand-effacing lesions which are characterized by localized degeneration of the microvilli, intimate contact between the bacteria and the infected cell, and the assembly of highly organized cytoskeletal structures in the epithelial cells just beneath the attached bacteria, forming cuplike pedestals (22,27,30). EPEC is also able to induce its internalization by nonphagocytic epithelial cells (2,15).…”

mentioning

confidence: 99%

Saccharomyces boulardiiPreserves the Barrier Function and Modulates the Signal Transduction Pathway Induced in EnteropathogenicEscherichia coli-Infected T84 Cells

Czerucka¹,

Dahan²,

et al. 2000

View full text Add to dashboard Cite

Use of the nonpathogenic yeastSaccharomyces boulardii is a thermophilic, nonpathogenic yeast administered in Western Europe for the prevention and treatment of a variety of diarrheal diseases (17, 29). However, the mechanisms by which S. boulardii controls diarrhea remain elusive. The efficacy of this yeast has been attributed to several of its properties, such as its effect on the mucosa leading to an increase in dissaccharidase activity (8) or stimulation of the immune response (7). In animals, administration of S. boulardii provides protection against intestinal lesions caused by several diarrheal pathogens (10,33). In vitro studies have demonstrated that S. boulardii exerts antagonistic activity against various bacterial pathogens (6). Recent studies have reported the adhesion of the Salmonella enterica serovars Typhimurium and Enteritis and of enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli to S. boulardii (24,25).EPEC is a major cause of diarrhea in the developing world (31, 34). The pathogenesis of EPEC infections involves a three-stage process. (i) EPEC adheres initially to intestinal epithelial cells in a pattern described as localized adherence (36). This pattern of adherence, characterized by microcolonies of bacteria associated with the epithelial cells, is dependent on the expression of the bacterial type IV bundle-forming pilus (BFP) (3). (ii) Next, the bacteria induce signal transduction pathways in host cells, leading to an elevation in the intracellular levels of Ca 2ϩ and inositol triphosphate (16, 23) and the phosphorylation of cellular proteins (4, 35, 41). (iii) These signaling events culminate in the formation of attachingand-effacing lesions which are characterized by localized degeneration of the microvilli, intimate contact between the bacteria and the infected cell, and the assembly of highly organized cytoskeletal structures in the epithelial cells just beneath the attached bacteria, forming cuplike pedestals (22,27,30). EPEC is also able to induce its internalization by nonphagocytic epithelial cells (2, 15).The aim of our study was to investigate in vitro the effect of S. boulardii against EPEC infection using the T84 cell line derived from a colon carcinoma. This cell line has been extensively used to elucidate the mechanism of EPEC-induced diarrhea. EPEC infection results in a modification of the T84 barrier function, characterized by a drop in transepithelial resistance, an increase in permeability, and modification of the distribution of the tight junction-associated protein 37). Our study reveals that S. boulardii maintains the barrier function and the viability of EPEC-infected T84 cells. Although the yeast does not modify the number of cell-associated bacteria, it reduces the number of intracellular bacteria. The phosphorylation of several proteins induced by EPEC in T84 cells is diminished in the presence of S. boulardii. Finally, the yeast interferes with the ERK1/2 mitogen-activated protein (MAP) kinase pathway that, as demonstrated in this study, is ...

show abstract

“…For example, initial engulfment of Yersinia, Neisseria, Listeria, and Streptococcus occurs via zipper-like receptor-mediated endocytosis (27,32,55), which is characterized by invagination of the host cell membrane at the site of bacterial attachment to the extent that the host cell membrane zips up around the entire surface of the bacterium (44). Enteropathogenic Escherichia coli (EPEC) is thought to be internalized by a similar mechanism subsequent to the formation of an adherence pedestal (6,71). In contrast, engulfment of Salmonella and Shigella occurs by macropinocytosis, involving the formation of host cell membrane ruffles (32,35).…”

mentioning

confidence: 99%

Specific Entry ofHelicobacter pyloriinto Cultured Gastric Epithelial Cells via a Zipper-Like Mechanism

et al. 2002

View full text Add to dashboard Cite

Although Helicobacter pylori has generally been considered an extracellular pathogen, a number of in vitro infection experiments and biopsy examinations have shown that it is capable of occasionally entering mammalian host cells. Here, we characterized this entry process by using AGS cells as a host cell model. In gentamicin protection-invasion assays, the number of H. pylori colonies recovered was lower than that for Salmonella enterica serovar Typhimurium X22, Escherichia coli expressing InvA, and Yersinia enterocolitica YO:9 grown at 25°C but higher than that for Neisseria gonorrhoeae VP1 and Y. enterocolitica YO:9 grown at 37°C. At the ultrastructural level, the entry process was observed to occur via a zipper-like mechanism. Internalized H. pylori was bound in tight LAMP-1-containing vacuoles in close association with condensed filamentous actin and tyrosine phosphorylation signals. Wortmannin, a potent inhibitor of phosphatidylinositol 3-kinase, and calphostin C, an inhibitor of protein kinase C, both inhibited the entry of H. pylori in a sensitive and dosedependent manner; however, the level of entry was enhanced by sodium vanadate, an inhibitor of tyrosine phosphatases and ATPases. Furthermore, the cytokine tumor necrosis factor alpha antagonized the entry of H. pylori into AGS cells. Collectively, these results demonstrate that the entry of H. pylori into AGS cells occurs via a zipper-like mechanism which involves various host signal transduction events.

show abstract

An endocytic process in HEp-2 cells induced by enteropathogenic Escherichia coli

Cited by 53 publications

References 13 publications

Signal transduction between enteropathogenic Escherichia coli (EPEC) and epithelial cells: EPEC induces tyrosine phosphorylation of host cell proteins to initiate cytoskeletal rearrangement and bacterial uptake

Signal transduction between enteropathogenic Escherichia coli (EPEC) and epithelial cells: EPEC induces tyrosine phosphorylation of host cell proteins to initiate cytoskeletal rearrangement and bacterial uptake

Saccharomyces boulardiiPreserves the Barrier Function and Modulates the Signal Transduction Pathway Induced in EnteropathogenicEscherichia coli-Infected T84 Cells

Specific Entry ofHelicobacter pyloriinto Cultured Gastric Epithelial Cells via a Zipper-Like Mechanism

Contact Info

Product

Resources

About