Apoptosis-inducing factor contributes to epithelial cell apoptosis induced by enteropathogenic Escherichia coli

2011 ◽  
Vol 89 (2) ◽  
pp. 143-148 ◽  
Author(s):  
Andrew N. Flynn ◽  
Arthur Wang ◽  
Derek M. McKay ◽  
Andre G. Buret
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Enteropathogenic Escherichia Coli ◽  
Epithelial Cell Apoptosis ◽  
Cellular Apoptosis ◽  
Apoptosis Inducing Factor

The mechanisms by which enteropathogenic Escherichia coli (EPEC) causes intestinal epithelial cell apoptosis remain unclear. We tested the hypothesis that apoptosis-inducing factor (AIF) is involved in apoptosis induced by EPEC. Infection of intestinal epithelial cells in vitro with EPEC led to the mitochondrial and cytosolic accumulation of AIF. This effect was partially dependent on caspase activity. Knockdown of AIF with siRNA blocked cellular apoptosis in response to EPEC infection, as assessed by poly(ADP-ribose) polymerase cleavage and oligonucleosome formation. Taken together, these data suggest that caspase-dependent mobilization of AIF contributes to EPEC-induced epithelial cell apoptosis.

scholarly journals Reovirus-Induced Apoptosis in the Intestine Limits Establishment of Enteric Infection

2018 ◽  
Vol 92 (10) ◽  
Author(s):  
Judy J. Brown ◽  
Sarah P. Short ◽  
Jennifer Stencel-Baerenwald ◽  
Kelly Urbanek ◽  
Andrea J. Pruijssers ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Oral Tolerance ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Enteric Infection ◽  
Intestinal Epithelial ◽  
Epithelial Cell Apoptosis ◽  
Induced Apoptosis

ABSTRACTSeveral viruses induce intestinal epithelial cell death during enteric infection. However, it is unclear whether proapoptotic capacity promotes or inhibits replication in this tissue. We infected mice with two reovirus strains that infect the intestine but differ in the capacity to alter immunological tolerance to new food antigen. Infection with reovirus strain T1L, which induces an inflammatory immune response to fed antigen, is prolonged in the intestine, whereas T3D-RV, which does not induce this response, is rapidly cleared from the intestine. Compared with T1L, T3D-RV infection triggered apoptosis of intestinal epithelial cells and subsequent sloughing of dead cells into the intestinal lumen. We conclude that the infection advantage of T1L derives from its capacity to subvert host restriction by epithelial cell apoptosis, providing a possible mechanism by which T1L enhances inflammatory signals during antigen feeding. Using a panel of T1L × T3D-RV reassortant viruses, we identified the viral M1 and M2 gene segments as determinants of reovirus-induced apoptosis in the intestine. Expression of the T1L M1 and M2 genes in a T3D-RV background was sufficient to limit epithelial cell apoptosis and enhance viral infection to levels displayed by T1L. These findings define additional reovirus gene segments required for enteric infection of mice and illuminate the antiviral effect of intestinal epithelial cell apoptosis in limiting enteric viral infection. Viral strain-specific differences in the capacity to infect the intestine may be useful in identifying viruses capable of ameliorating tolerance to fed antigen in autoimmune conditions like celiac disease.IMPORTANCEAcute viral infections are thought to be cleared by the host with few lasting consequences. However, there may be much broader and long-lasting effects of viruses on immune homeostasis. Infection with reovirus, a common, nonpathogenic virus, triggers inflammation against innocuous food antigens, implicating this virus in the development of celiac disease, an autoimmune intestinal disorder triggered by exposure to dietary gluten. Using two reovirus strains that differ in the capacity to abrogate oral tolerance, we found that strain-specific differences in the capacity to replicate in the intestine inversely correlate with the capacity to induce apoptotic death of intestinal epithelial cells, providing a host-mediated process to restrict intestinal infection. This work contributes new knowledge about virus-host interactions in the intestine and establishes a foundation for future studies to define mechanisms by which viruses break oral tolerance in celiac disease.

IL-10 modulates intestinal damage and epithelial cell apoptosis in T cell-mediated enteropathy

2004 ◽  
Vol 287 (3) ◽  
pp. G599-G604 ◽  
Author(s):  
Pengfei Zhou ◽  
Cathy Streutker ◽  
Rajka Borojevic ◽  
Yufa Wang ◽  
Ken Croitoru
Keyword(s):  
T Cell ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cells ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Intestinal Tissue ◽  
Epithelial Cell Apoptosis

In vivo T cell activation by anti-CD3 monoclonal antibody (mAb) results in intestinal damage characterized by loss of villi and epithelial cell apoptosis. The role of the increased interleukin (IL)-10 released during this process is not clear. We assessed the effects of IL-10 on T cell-induced mucosal damage in vivo using IL-10-deficient C57BL/6 [IL-10 knockout (KO)] mice. IL-10 KO and wild-type C57BL/6 mice were injected with anti-CD3 mAb and observed for diarrhea. Changes in serum cytokine levels were measured by ELISA. Histological changes and epithelial cell apoptosis were analyzed on hematoxylin- and eosin-stained tissue sections. Fas expression on intestinal epithelial cells was assessed by flow cytometry analysis of freshly isolated intestinal epithelial cells. Anti-CD3-treated IL-10 KO mice developed more severe diarrhea, a greater loss of intestinal villi, and an increase in the numbers of apoptotic cells in the crypt epithelium. This difference in IL-10 KO mice was associated with an increase in serum tumor necrosis factor-α and interferon-γ levels and with an increase in Fas expression on fresh, isolated, small intestinal epithelial cells. In addition, the enhanced intestinal tissue damage induced by anti-CD3 in IL-10 KO mice was significantly diminished by treatment with recombinant murine IL-10. Therefore, the lack of IL-10 allowed for an increased T cell-induced intestinal tissue damage, and this was associated with an increase in T cell cytokine release and an increase in epithelial cell Fas expression.

scholarly journals TNF-αneutralization ameliorates the severity of murine Crohn's-like ileitis by abrogation of intestinal epithelial cell apoptosis

2003 ◽  
Vol 100 (14) ◽  
pp. 8366-8371 ◽  
Author(s):  
Marco Marini ◽  
Giorgos Bamias ◽  
Jesús Rivera-Nieves ◽  
Christopher A. Moskaluk ◽  
Sharon B. Hoang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Apoptosis
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