scholarly journals Bacteroides fragilis toxin stimulates intestinal epithelial cell shedding and  -secretase-dependent E-cadherin cleavage

2007 ◽  
Vol 120 (20) ◽  
pp. 3713-3713
Author(s):  
S. Wu ◽  
K.-J. Rhee ◽  
M. Zhang ◽  
A. Franco ◽  
C. L. Sears
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Bacteroides Fragilis ◽  
Intestinal Epithelial ◽  
Cell Shedding ◽  
E Cadherin

scholarly journals Bacteroides fragilis toxin stimulates intestinal epithelial cell shedding and  -secretase-dependent E-cadherin cleavage

2007 ◽  
Vol 120 (11) ◽  
pp. 1944-1952 ◽  
Author(s):  
S. Wu ◽  
K.-J. Rhee ◽  
M. Zhang ◽  
A. Franco ◽  
C. L. Sears
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Bacteroides Fragilis ◽  
Intestinal Epithelial ◽  
Cell Shedding ◽  
E Cadherin

scholarly journals Epidermal growth factor suppresses intestinal epithelial cell shedding through a MAPK-dependent pathway

2016 ◽  
Vol 130 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Jennifer C. Miguel ◽  
Adrienne A. Maxwell ◽  
Jonathan J. Hsieh ◽  
Lukas C. Harnisch ◽  
Denise Al Alam ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Epidermal Growth Factor ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Epidermal Growth ◽  
Cell Shedding ◽  
Dependent Pathway

scholarly journals Induction of Persistent Colitis by a Human Commensal, Enterotoxigenic Bacteroides fragilis, in Wild-Type C57BL/6 Mice

2009 ◽  
Vol 77 (4) ◽  
pp. 1708-1718 ◽  
Author(s):  
Ki-Jong Rhee ◽  
Shaoguang Wu ◽  
XinQun Wu ◽  
David L. Huso ◽  
Baktiar Karim ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Bacteroides Fragilis ◽  
Receptor Activation ◽  
Intestinal Epithelial ◽  
Wild Type ◽  
Bowel Diseases ◽  
Specific Pathogen ◽  
E Cadherin

ABSTRACT Enterotoxigenic Bacteroides fragilis (ETBF) causes diarrhea and is implicated in inflammatory bowel diseases and colorectal cancer. The only known ETBF virulence factor is the Bacteroides fragilis toxin (BFT), which induces E-cadherin cleavage, interleukin-8 secretion, and epithelial cell proliferation. A murine model for ETBF has not been characterized. Specific pathogen-free (SPF) C57BL/6J or germfree 129S6/SvEv mice were orally inoculated with wild-type ETBF (WT-ETBF) strains, a nontoxigenic WT strain of B. fragilis (WT-NTBF), WT-NTBF overexpressing bft (rETBF), or WT-NTBF overexpressing a biologically inactive mutated bft (rNTBF). In SPF and germfree mice, ETBF caused colitis but was lethal only in germfree mice. Colonic histopathology demonstrated mucosal thickening with inflammatory cell infiltration, crypt abscesses, and epithelial cell exfoliation, erosion, and ulceration. SPF mice colonized with rETBF mimicked WT-ETBF, whereas rNTBF caused no histopathology. Intestinal epithelial E-cadherin was rapidly cleaved in vivo in WT-ETBF-colonized mice and in vitro in intestinal tissues cultured with purified BFT. ETBF mice colonized for 16 months exhibited persistent colitis. BFT did not directly induce lymphocyte proliferation, dendritic cell stimulation, or Toll-like receptor activation. In conclusion, WT-ETBF induced acute then persistent colitis in SPF mice and rapidly lethal colitis in WT germfree mice. Our data support the hypothesis that chronic colonization with the human commensal ETBF can induce persistent, subclinical colitis in humans.

scholarly journals The early life microbiota protects neonatal mice from pathological small intestinal epithelial cell shedding

2019 ◽  
Author(s):  
Kevin R Hughes ◽  
Z Schofield ◽  
MJ Dalby ◽  
S Caim ◽  
L Chalklen ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Gut Microbiota ◽  
Early Life ◽  
Intestinal Epithelial Cell ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Neonatal Mice ◽  
Small Intestinal ◽  
The Impact ◽  
Cell Shedding

AbstractThe gut microbiota plays a crucial role in regulating and maintaining the epithelial barrier, particularly during early life. Notably, patients with chronic intestinal inflammation have a dysregulated process of renewal and replenishment of the intestinal epithelial cell (IEC) barrier, which is linked to disturbances in the gut microbiota. To date, there are no studies focussed on understanding the impact of inflammatory cell shedding events during the early life developmental window, and which host and microbial factors mediate these responses. Here we sought to determine pathological cell shedding outcomes throughout the postnatal developmental period (day 14, 21, 29 and week 8). Surprisingly neonatal mice (day 14 and 21) were highly refractory to induction of cell shedding after intraperitoneal administration of LPS, with day 29 mice showing strong pathological responses, more similar to those observed in adult mice. These differential responses were not linked to defects in the cellular mechanisms and pathways known to regulate cell shedding responses, although we did observe that neonatal mice had elevated anti-inflammatory (IL-10) responses. Notably, when we profiled microbiota and metabolites from these mice, we observed significant alterations. Neonatal mice had high relative abundances of Streptococcus, Escherichia and Enterococcus and increased primary bile acids. In contrast, older mice were dominated by Candidatus Arthromitus, Alistipes and Lachnoclostridium, and had increased concentrations of SCFAs and methyamines. Faecal microbiota transplant (FMT) and antibiotic studies confirmed the importance of early life gut microbiota in cell shedding responses. In these studies, neonates treated with antibiotics restored LPS-induced small intestinal cell shedding, whereas adult FMT alone had no effect. Our findings further support the importance of the early life window for microbiota-epithelial interactions in the presence of inflammatory stimuli and highlight areas for further investigation to probe underlying mechanisms to drive therapeutic development within the context of chronic inflammatory intestinal diseases.

EGF suppresses intestinal epithelial cell shedding both in vitro and in vivo via a MEK/ERK dependent pathway

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Mark R Frey ◽  
Jennifer C Miguel ◽  
Ching‐Ling Lien ◽  
Alastair J Watson
Keyword(s):  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Shedding ◽  
Dependent Pathway
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