ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Enteropathogenic E. coli-induced barrier function alteration is not a consequence of host cell apoptosis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Alternatives to animal models in gastroenterology and hepatology research.Frontiers in pharmacology · 2026Review
- Mitotic Arrest-Deficient 2 Like 2 (MAD2L2) Interacts withLife (Basel, Switzerland) · 2021Article
- Pan-caspase inhibition as a potential host-directed immunotherapy against MRSA and other bacterial skin infections.Science translational medicine · 2021Article
- EnterohemorrhagicFrontiers in cell and developmental biology · 2020Article
- Modulation of Intestinal Paracellular Transport by Bacterial Pathogens.Comprehensive Physiology · 2018Review
- The EspF N-Terminal of EnterohemorrhagicFrontiers in cellular and infection microbiology · 2017Article
- Necrotizing enterocolitis in a mouse model leads to widespread renal inflammation, acute kidney injury, and disruption of renal tight junction proteins.Pediatric research · 2015Article
- Claudin-4 undergoes age-dependent change in cellular localization on pig jejunal villous epithelial cells, independent of bacterial colonization.Mediators of inflammation · 2015Article
- Pathogenesis of human enterovirulent bacteria: lessons from cultured, fully differentiated human colon cancer cell lines.Microbiology and molecular biology reviews : MMBR · 2013Review
- Bifidobacteria stabilize claudins at tight junctions and prevent intestinal barrier dysfunction in mouse necrotizing enterocolitis.The American journal of pathology · 2013Article
- Differential targeting of the E-Cadherin/β-Catenin complex by gram-positive probiotic lactobacilli improves epithelial barrier function.Applied and environmental microbiology · 2012Article
- Higher molecular weight polyethylene glycol increases cell proliferation while improving barrier function in an in vitro colon cancer model.Journal of biomedicine & biotechnology · 2011Article
- The EspF effector, a bacterial pathogen's Swiss army knife.Infection and immunity · 2010Article
- Enteric pathogens and gut function: Role of cytokines and STATs.Gut microbes · 2010Article
- The enteropathogenic E. coli effector EspF targets and disrupts the nucleolus by a process regulated by mitochondrial dysfunction.PLoS pathogens · 2010Article
- Disruption of occludin function in polarized epithelial cells activates the extrinsic pathway of apoptosis leading to cell extrusion without loss of transepithelial resistance.BMC cell biology · 2009Article
- Innate immune recognition of infected apoptotic cells directs T(H)17 cell differentiation.Nature · 2009Article
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Authors and funding
5 authors.
Funding
Abstract
Enteropathogenic Escherichia coli (EPEC) is a diarrheagenic pathogen that perturbs intestinal epithelial function. Many of the alterations in the host cells are mediated by effector molecules that are secreted directly into epithelial cells by the EPEC type III secretion system. The secreted effector molecule EspF plays a key role in redistributing tight junction proteins and altering epithelial barrier function. EspF has also been shown to localize to mitochondria and trigger membrane depolarization and eventual host cell death. The relationship, if any, between EspF-induced host cell death and epithelial barrier disruption is presently not known. Site-directed mutation of leucine 16 (L16E) of EspF impairs both mitochondrial localization and consequent host cell death. Although the mutation lies within a region critical for type III secretion, EspF(L16E) is secreted efficiently from EPEC. Despite its inability to promote cell death, EspF(L16E) was not impaired for tight junction alteration or barrier disruption. Consistent with this, the pan-caspase inhibitor Q-VD-OPH, despite reducing EPEC-induced host cell death, had no effect on infection-mediated barrier function alteration. Thus EPEC alters the epithelial barrier independent of its ability to induce host cell death.
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