Intestinal Epithelial Cell Response to Clostridium difficile Flagella

2016 ◽  
pp. 103-116 ◽  
Author(s):  
Jameel Batah ◽  
Imad Kansau
Keyword(s):  
Epithelial Cell ◽  
Clostridium Difficile ◽  
Cell Response ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial

scholarly journals Intrarectal Instillation of Clostridium difficile Toxin A Triggers Colonic Inflammation and Tissue Damage: Development of a Novel and Efficient Mouse Model of Clostridium difficile Toxin Exposure

2012 ◽  
Vol 80 (12) ◽  
pp. 4474-4484 ◽  
Author(s):  
Simon A. Hirota ◽  
Vadim Iablokov ◽  
Sarah E. Tulk ◽  
L. Patrick Schenck ◽  
Helen Becker ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Clostridium Difficile ◽  
Inflammatory Mediators ◽  
Tissue Damage ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Toxin A ◽  
Colonic Inflammation ◽  
Content Type ◽  
Clostridium Difficile Toxin

ABSTRACTClostridium difficile, a major cause of hospital-acquired diarrhea, triggers disease through the release of two toxins, toxin A (TcdA) and toxin B (TcdB). These toxins disrupt the cytoskeleton of the intestinal epithelial cell, increasing intestinal permeability and triggering the release of inflammatory mediators resulting in intestinal injury and inflammation. The most prevalent animal model to study TcdA/TcdB-induced intestinal injury involves injecting toxin into the lumen of a surgically generated “ileal loop.” This model is time-consuming and exhibits variability depending on the expertise of the surgeon. Furthermore, the target organ ofC. difficileinfection (CDI) in humans is the colon, not the ileum. In the current study, we describe a new model of CDI that involves intrarectal instillation of TcdA/TcdB into the mouse colon. The administration of TcdA/TcdB triggered colonic inflammation and neutrophil and macrophage infiltration as well as increased epithelial barrier permeability and intestinal epithelial cell death. The damage and inflammation triggered by TcdA/TcdB isolates from the VPI and 630 strains correlated with the concentration of TcdA and TcdB produced. TcdA/TcdB exposure increased the expression of a number of inflammatory mediators associated with human CDI, including interleukin-6 (IL-6), gamma interferon (IFN-γ), and IL-1β. Finally, we were able to demonstrate that TcdA was much more potent at inducing colonic injury than was TcdB but TcdB could act synergistically with TcdA to exacerbate injury. Taken together, our data indicate that the intrarectal murine model provides a robust and efficient system to examine the effects of TcdA/TcdB on the induction of inflammation and colonic tissue damage in the context of human CDI.

Real-Time Cell Analysis for Monitoring Cholera Toxin-Induced Human Intestinal Epithelial Cell Response

2014 ◽  
Vol 70 (4) ◽  
pp. 536-543 ◽  
Author(s):  
Julian Ye ◽  
Yun Luo ◽  
Weijia Fang ◽  
Junhang Pan ◽  
Zheng Zhang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cholera Toxin ◽  
Real Time ◽  
Cell Response ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Cell Analysis ◽  
Human Intestinal Epithelial Cell

Clostridium difficile Toxin A Induces Intestinal Epithelial Cell Apoptosis and Damage: Role of Gln and Ala-Gln in Toxin A Effects

2005 ◽  
Vol 50 (7) ◽  
pp. 1271-1278 ◽  
Author(s):  
Gerly A. C. Brito ◽  
Benedito Carneiro-filho ◽  
Reinaldo B. Oriá ◽  
Raul V. Destura ◽  
Aldo A. M. Lima ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Clostridium Difficile ◽  
Cell Apoptosis ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Toxin A ◽  
Epithelial Cell Apoptosis ◽  
Clostridium Difficile Toxin ◽  
Clostridium Difficile Toxin A
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