Escherichia coli STb toxin induces apoptosis in intestinal epithelial cell lines

Syed, Huma; Dubreuil, J. Daniel

doi:10.1016/j.micpath.2012.06.003

Cited by 18 publications

(14 citation statements)

References 161 publications

(234 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…STb enterotoxin was produced as described previously (30). Briefly, E. coli HB101 strains harboring pMal-STb, a plasmid encoding wild-type STb protein fused to the maltose binding protein, were used.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Escherichia coli Heat-Stable Toxin b Impairs Intestinal Epithelial Barrier Function by Altering Tight Junction Proteins

Mukiza

Dubreuil

2013

Infect Immun

Self Cite

View full text Add to dashboard Cite

Escherichia coli heat-stable toxin b (STb) causes diarrhea in animals. STb binds to sulfatide, its receptor, and is then internalized. In the cytoplasm, through a cascade of events, STb triggers the opening of ion channels, allowing ion secretion and water loss and leading to diarrhea. Tight junctions (TJs) are well known for controlling paracellular traffic of ions and water by forming a physical intercellular barrier in epithelial cells, and some bacterial toxins are known to affect adversely TJs. The present study aimed at determining the effect of STb on TJs. T84 cells were treated for 24 h with purified STb and a nontoxic STb mutant (D30V). Transepithelial resistance (TER), paracellular flux marker, and confocal microscopy were used to analyze the effect of STb on TJs. Purified STb caused a significant reduction of TER parallel to an increase in paracellular permeability compared to the results seen in untreated cells or mutant D30V. The increased paracellular permeability was associated with a marked alteration of F-actin stress fibers. F-actin filament dissolution and condensation were accompanied by redistribution and/or fragmentation of ZO-1, claudin-1, and occludin. These changes were also observed following treatment of T84 cells with an 8-amino-acid peptide found in the STb sequence corresponding to a consensus sequence of Vibrio cholerae Zot toxin. These effects were not observed with a scrambled peptide or mutant D30V. Our findings indicate that STb induces epithelial barrier dysfunction through changes in TJ proteins that could contribute to diarrhea.

show abstract

Section: Methodsmentioning

confidence: 99%

“…3B and E). These structural changes are characteristic of preapoptotic alterations consisting of chromatin condensation followed by DNA fragmentation (30). STb causes disassembly of TJ proteins and cellular morphology.…”

Section: Determination Of Assay Parametersmentioning

confidence: 99%

Escherichia coli Heat-Stable Toxin b Impairs Intestinal Epithelial Barrier Function by Altering Tight Junction Proteins

Mukiza

Dubreuil

2013

Infect Immun

Self Cite

View full text Add to dashboard Cite

show abstract

“…In human (human colon tumor, HRT-18) and animal (rat ileum epithelium, IEC-18) cell lines, caspase-9, the initiator of mitochondrion-mediated apoptosis and caspase-3, an effector of caspase-9, were both activated following STb intoxication (490). DNA fragmentation was observed as well as condensation and fragmentation of nuclei.…”

Section: Stbmentioning

confidence: 99%

Animal EnterotoxigenicEscherichia coli

2016

Self Cite

View full text Add to dashboard Cite

Enterotoxigenic Escherichia coli (ETEC) is the most common cause of E. coli diarrhea in farm animals. ETEC are characterized by the ability to produce two types of virulence factors; adhesins that promote binding to specific enterocyte receptors for intestinal colonization and enterotoxins responsible for fluid secretion. The best-characterized adhesins are expressed in the context of fimbriae, such as the F4 (also designated K88), F5 (K99), F6 (987P), F17 and F18 fimbriae. Once established in the animal small intestine, ETEC produces enterotoxin(s) that lead to diarrhea. The enterotoxins belong to two major classes; heat-labile toxin that consist of one active and five binding subunits (LT), and heat-stable toxins that are small polypeptides (STa, STb, and EAST1). This chapter describes the disease and pathogenesis of animal ETEC, the corresponding virulence genes and protein products of these bacteria, their regulation and targets in animal hosts, as well as mechanisms of action. Furthermore, vaccines, inhibitors, probiotics and the identification of potential new targets identified by genomics are presented in the context of animal ETEC.

show abstract

“…ETEC colonizes the intestine by fimbrial adhesins (K88/F4, K99/F5, 987P/F6, F41/F7 and F18), and then produces enterotoxins, such as heat labile (LT), heat-stable (STa and STb), and entero-aggregative Escherichia coli heat-stable enterotoxin-1, which leads to excessive loss of fluids and electrolytes resulting in profuse diarrhea, frequently without histological lesions (1,2). The alterations of intestinal function following ETEC colonization are widely investigated, including autophagy (3), immune responses (4-7), nutrient absorption (8), barrier integrity (9)(10)(11) and apoptosis (12,13).…”

Section: Introductionmentioning

confidence: 99%

Enterotoxigenic Escherichia coli infection alters intestinal immunity in mice

Yang

Xiao

Liu

et al. 2016

Molecular Medicine Reports

View full text Add to dashboard Cite

Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhea in humans and piglets. However, research regarding alterations of intestinal immunity following ETEC infection remains limited and the results controversial. The present study investigated the effects of ETEC on the expression levels of pro‑inflammatory cytokines and innate immune regulators from plasma cells, goblet cells and Paneth cells, and the activation of toll‑like receptor 4-nuclear factor (NF)‑κB and mitogen‑activated protein kinase (MAPK) pathways using reverse transcription‑quantitative polymerase chain reaction and western blot analysis, in a mouse model infected with a porcine isolated ETEC strain. ETEC infection significantly reduced the expression of pro‑inflammatory cytokines in the mouse jejunum (P<0.05). Additionally, ETEC infection significantly affected the expression of immune regulators of plasma cells, goblet cells and Paneth cells in the mouse intestine (P<0.05). ETEC influenced the intestinal immunity via the NF‑κB and MAPK signaling pathways. In conclusion, ETEC colonization affects intestinal immunity as observed in a mouse model. This study provides a greater understanding of the pathogenesis of ETEC infection in animals and humans.

show abstract

Escherichia coli STb toxin induces apoptosis in intestinal epithelial cell lines

Cited by 18 publications

References 161 publications

Escherichia coli Heat-Stable Toxin b Impairs Intestinal Epithelial Barrier Function by Altering Tight Junction Proteins

Escherichia coli Heat-Stable Toxin b Impairs Intestinal Epithelial Barrier Function by Altering Tight Junction Proteins

Animal EnterotoxigenicEscherichia coli

Enterotoxigenic Escherichia coli infection alters intestinal immunity in mice

Contact Info

Product

Resources

About